Deborah Mash’s Brain

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

All Rights Reserved

CHAPTER 18: Deborah Mash’s Brain

In March, 1994, in strictest secrecy, Howard Lotsof re-instituted treatments of addict volunteers in an ultramodern hospital in Panama City, with pre-treatment work-ups at the University of Miami. But this time, with hush-hush clearance by the Panamanian Ministry of Health, hourly bloodsamples would be flown directly to the Addiction Research Center in Baltimore, affording NIDA scientists a window to observe the pharmacokinetics of Ibogaine for the first time in humans. Grudzinskas was once again fulltime head of MDD, following the appointment of Alan Leshner as Director of NIDA in February, and Frank Vocci, true to his word, was moving into high gear.

Among these new treatments was Nancy, a third-timer who’d become re-addicted since the treatments stopped. Nancy’s opiate experience began with access to someone else’s take-home methadone–she was on 100 mgs daily plus other drugs.

Her first Ibogaine was in Holland, 25 mg./kg., during the same Jan. ’93 treatments–except that she declined to be videotaped by ABC “Day One.” Two 1/2 mos. later, at the end of March, ’93, she required re-treatment, with 29-31 mg./kg. But progress against her addiction didn’t end her health problems; during the summer she stopped menstruating.

Her third treatment, in March of ’94, actually consisted of two administrations–10 mg./kg. on the 25th and 20 mg./kg on the 28th–since Howard and the treatment team were leery of giving the whole 30 mgs at once in light of known female sensitivity. A painstaking checkup at the University of Miami had failed to detect any physical basis for her complaints of recurrent intestinal malaise and diarrhea that would preclude more Ibogaine. Recovery was uneventful, although the problem with her insides didn’t get any better. She flew straight back to the New York area, and was examined 5 days after treatment at Jackson Memorial Hospital.

On April 21, though, she flew back down to Miami for a medical exam at the U. of Miami–part of the followup to her Panamanian re-treatment. No ill-effects of Ibogaine–but still no explanation of her diarrhea and recurrent vomiting. She was released from the hospital. Much later that evening she was found dead at the apartment where she was staying, collapsed in her vomit. Estimated time of death, 9:40 PM.

By coincidence, Nancy died in the only place in the country where bodies routinely go to Dr. Lee Hearn, who happens to be Dade County medical examiner as well as the member of Deborah Mash’s team who discovered the active metabolite noribogaine. The autopsy–much more exhaustive than in previous deaths–found no discernible link to Nancy’s recent re-treatment, establishing cause of death as mesenteric artery thrombosis (heart attack) associated with small bowel infarction (blockage), complicated by a general “hypercoagulable state” of the blood due to chronic infection in the thigh.

The Institutional Review Board of University of Miami hospital reviewed all this and concurred: death was not caused by Ibogaine. So Deborah Mash wound up with the one and only body in existence of a woman who certifiably didn’t die of Ibogaine yet had received multiple Ibogaine exposures in the previous 14 months. And the brain was in pristine condition, so that researchers could look for traces of non-lethal neuro-toxicity, the kind that ordinarily never shows up in behavior, and goes undetected. Brains with just the right drug history are hard to come by.

Meanwhile, it was deemed safe to go ahead in Panama with more male treatments, in July. After talking with Anne Shulgin about the “doorway of light,” Mash did make one change in her protocol. She drew up a contract all prospective treatments have to sign “agreeing to come back.” To this day, she says Nicola K’s boyfriend insists she did not die of Ibogaine toxicity, but “found the doorway and went through it of her own free will.”

In late September, Sisko and Rommell flew to Panama City, to be with Howard and Deborah Mash as they treated 3 more male addicts, including an older heroin addict who was shooting $5,000 a month. Also a younger crackhead who was basing $1,000 a week, so that his wealthy family could well afford the Ibogaine. The kid had a full-blown experience. He described encountering Bwiti as a half million year old Black Man in a Desert, but relapsed almost as soon as he got home. The older guy’s liver function improved.

Howard and the local doctors did a press conference announcing Panamanian government approval of experimental Ibogaine.

At the very end of October David Goldstein showed up at 9 Bleecker with important news: a researcher named Poppik* had discovered Ibogaine activity at the same NMDA (N-Methy-D-Aspartate) receptor as harmaline (Woods, 1982).

Popik characterized Ibogaine and its cogeners including harmaline as “noncompetitive” NMDA antagonists [binding only one micron more to the NMDA receptor, according to Molliver, than to the kappa opiate receptor]. In effect they are more like nor-harman, the neuro-transmitter associated with REM, eidetic memory and the NDE, as opposed to serotonergic indole ring alkaloids like LSD.

In David’s materials on the NMDA receptor were papers on the potent anti-stroke medication diszolcilpine (MK801). Both Ibogaine and harmaline displace the somewhat oneiric MK801, suggesting a common mechanism of action. Daily administration of MK801 attenuated both tolerance to and dependence upon alcohol and morphine.*** Also, MK 801 has been also found to inhibit the supersensitization to cocaine that sometimes occurs with tolereance to cocaine.**

MK 801 is a hallucinogen — more related to phencyclidine and ketamine than Ibogaine/harmaline. Yet FDA approved it, because an injection of MK801, even half an hour after a stroke, by blocking flow of potassium, sodium and calcium ions into brain cells, interferes with the normal “glutamate cascade” that fuels neurologic stroke damage, cutting it 50 to 75%.

This is important for understanding not just Ibogaine, but how “opium dreams” and delerium tremens may actually represent the neuro-protective activity of nor-harman, which has been implicated by Dzoljic et al as “endogenous Ibogaine.”

Ordinarily, NMDA receptor-channels are clogged by a bulky Magnesium ion (see illustration), and may not even play a role in normal synaptic transmission. A number of researchers**** are looking at the role of calcium influx in potentiation and growth, i.e, in long-lasting increases in nerve cell communication within the synapses.

In “Quantum Coherence in Microtubules: A Neural Basis for Emergent Consciousness?,” Stuart Hameroff explains that consciousness itself emerges from a critical level of coherence of quantum-level events in cytoskeletal microtubules within neurons–that each microtube tranforms disordered molecular, thermal or electromagnetic energy into coherent photons within its hollow core, which penetrate without loss along the microtubule in a quantum phenomenon called self-induced transparency, manifesting a collective dynamics called super-radiance–involving synchronous, self-organizing firing of widely distributed neurons.* Our neurons, like swarms of fireflies, wax and wane together in quantum simultaneity, even though cell-to-cell, receptor-based communication must be electro-chemical, and therefore slower.

NMDA-mediated calcium influx induces changes in the spiny protrusions of dendrites, which receive chemical signals, while NMDA also a) stimulates post-synaptic release of arachidonic acid, a fatty acid that travels backward across synapses to presynaptic neurons and increases their output of neuro-transmitter, increasing synaptic strength; and b) may cause the enzyme protein kinase C to move from the cytoplasm out to the membrane where it phosphorylates protein growth. This new “hardwiring” allows the neuron to download the day’s short-term recptor memory into long-term cellular memory–clearing up the recptors, down-modulating toterance and supersensitivity.

To reconcile myriad conflicting receptor impulses requires more than blind tabulation, though. Remember that neurons are fiber-optic. Like any good neuro-transmitter, the body uses nor-harman to do a number of jobs–dreaming, waking REM, the NDE, even the DTs–which involve visualization, so that impulse and counter-impulse are played out in the REM circuitsand choices may be (semi)consciously made, not blindly tabulated.

A clue to the mechanism here came from Molliver, who recounts an experiment in which Llinas briefly exposed vermal cerebellar purkinje cells to harmaline–immediately “washing” his sample to remove all traces of harmaline. The purkinjes continued firing for 6 hrs. from this brief exposure–as if transparency in microtubules had been altered directly. Also, instead of blocking the NMDA receptor completely, the “flickering” effect of the harmaline (and iboga, and nor-harman during REM) allows a trickle of calcium in (since too much causes cell death)–to be processed, under the apparenmt direction of the REM circuits, into new hardwiring for your neurons.

This means that there’s no natural recovery without REM action on jaded receptors, turning short-term into long-term memory–without “maturing out.” And six hours of Ibogaine is like six months of REM. Chaotically (yet not randomly, since this chaos has personality), by calceous accretion of dendrites and microtubules, Ibogaine-fired information is not only retrieved but also (contrary to reigning 12-step paradigm) generated–created from connections that were not there before.

Ibogaine’s ‘stroboscopic’ effect–by almost but not quite blockading calcium influx at the NMDA site–seems to keep a feedback loop open which enables the body to “learn” its way out of withdrawal and craving. “Compared with the effects of harmaline,” observes Goutarel, “the fantasy evoked by Ibogaine is easier for the subject to manipulatee… so that, more often than with other drugs, they can stop to contemplate a scene, go back, explore an alternative in a given sequence, bring a previous scene back to life, etc.”

The key is “sensitive dependence on initial conditions,” which vastly multiplies the initial will of the addict to get better because dendrite/ micro-tubule accumulation has a built-in multiplier effect, an effect that’s not supposed to get out of control as long as they follow the red road.*** [perhaps because neurons must snag iron ions from the blood to keep the calcium activity in check].*

The Nganga say the red road is the best and safest way to the Village of the Ancestors. The first appearance of Bwiti as guide/gatekeeper is usually as a familiar elder or trusted ancestor. And this had been the thing Sisko emphasized, quoting Goutarel in response to Dana, in late September as they were returning to his house at the end of their long rap about harmaline and Ibogaine as sacraments: “For various reasons, poor preparation, inadequate motivation, fear, psychosis, neurosis–certain subjects are unable to get past this critical phase;” and cited the need for the neophyte to be “watched constantly by his ‘mother,’ who regulates his psychophysiological reactions to prevent him from letting terrifying phantoms interfere, for they would lead him down the wrong path, down the road of death.”

Later, on the other hand, after reviewing data on the NMDA receptor, Dana said to Sisko, “You know, if you’re being crucified, it makes perfect sense to take an anti-stroke medication. Harmala ought to stop the glutamate cascade–it binds to the same NMDA receptor as MK-801!”

In the beginning of November the Republicans won the election. Instead of focusing on AIDS and Ibogaine, Lee Brown had listened to CASA, Sue Rusche, and the Partnership for a Drug Free America: When in doubt, bash pot. Their idea of a big media event for the final days of the campaign was a highly telegenic Clinton speech to some schoolkids in Mass, in which he apologized even for not inhaling. Clips of that ran all day on CNN, inspiring 3-5 % of the electorate not to vote–since who or what was there to vote for. Post-election analysis concluded GOP carved out their narrow statistical victory not because of more Republicans, but because significant numbers of Democrats, in disgust, didn’t bother to vote.

The full impact of the 1994 election had not really sunk in when drug reformers gathered in D.C for the annual conference of the Drug Policy Foundation. One of the hottest workshops was the Ibogaine panel, starring Deborah Mash, with a ton of new data.

Mash revealed that Ibogaine blood concentrations reach a low peak from 2 to 4 hrs (during the visualizations), then rapidly fall off–de-methylated by the liver into the longer-acting, water-soluable noribogaine (termed m-1, or metabolite-one)–which peaks more sharply at 4 hrs. and slowly descends during the cognitive evaluation and insomnia phases. Somehow, she indicated, noribogaine may be hanging around the metabolism for some time–perhaps during the several weeks post-treatment when Ibogaine subjects are working off their REM-surplus and don’t sleep much. In fact, Mash’s team suspects noribogaine is Stanley Glick’s elusive, long-acting metabolite–that it was noribogaine which up until 4 months after her first treatment, made Geerte F. “experience colors and light very intensely”–that noribogaine was in fact responsible for the “Ibogaine-aftereffect” which Geerte experienced as “blockading craving until it wore off.”

Mash also announced her team had confirmed the discovery of Popkik, et al, that Ibogaine was found to key into the NMDA receptor. Activity at this receptor is an important key to understanding how Ibogaine actually averts braincell loss from excito-toxic delirium tremens or cold turkey withdrawal. It’s also an important clue to what can go wrong–too much glutamate and too much calcium cause excito-toxicity, and apoptosis–cell death.

Another discovery of the Mash team was Ibogaine binding at a third site–the muscarinic acetylcholine receptor–even weaker than at thekappa opiate or NMDA receptors. This is a post-synaptic receptor, i.e, it acts presumably by up-modulating reception of pre-synaptic acetylcholine activity. Acetylcholine is the neuro-transmitter for all sorts of muscular activity (heartbeat, etc.), but it is also an important neuro-transmitter, especially for sleep, REM, and so-on. Muscarine is the active, non-psychedelic component of amanita muscaria,* and is present, according the Sanchez-Ramos, in a number of substances used in traditional divination, such as datura. The Viking Berserkers used it just before battle not to trip, but because muscarinic acid causes bursts of action, and rage. In the REM circuits, the giant pontine cells [see illustration:] of the hippocampus where cerebellar acetyl-choline activity is shunted during REM, it is expressed as tremor because one’s responses are part of the dream–generating the “REM twitch.”

The other big revelation at the DPF Conference for Ibogaine-watchers came from Dr. Todd Mikurya, who had a letter from Defense Secretary William Perry declassifying records of all chemical research prior to 1968, including psychedelic research in humans. Dr. Todd went personally with a delegation of relatives of victims of various accidents and experiments over the lost 40 years, and met at Edgewood Arsenal with a bevy of Army brass headed by a Colonel. He couldn’t get access to the locked CIA facility at Edgewood where the Ibogaine records would be, however, without parallel clearance from the Director of the CIA. Curtis Wright was informed that FDA or NIDA could go ahead on their own and try–armed with the Perry letter–to get CIA to release their archives on the work of Isbell and others.

In December, Beal flew to spend Christmas in Germany with Georg Behr, who was just finishing up the new improvedVan Hanf Ist Die Rede. Behr was certain the last word on Ibogaine and the opiate receptors was not in, recalling that Sanchez-Ramos had told him just a few months earlier that his previous intuition that Ibogaine must generate some kind of opioid receptor activity besides the kappa had been a “good clue.”

In January, as the new Congress took its seats intent on enacting Gingrich’s gameplan for the first 100 days, the FDA and NIH huddled to consider threats that they might be abolished, or severely neutered. All the opponents of going forward with NIDA’s first Ibogaine trial, the NIDA old guard who disbelieved an interrupter was even possible, took their cue to come forward, to lobby Alan Leshner to stop it. Leshner ordered a complete review of MDD’ s Ibogaine Project by a new panel, of “outside consultants” including foremost critics like Reese Jones, Charles Gorodetzky, et al.

The first clue activists had something was up came when Curtis Wright, after telling them another NIDA design session was in the works, said MDD had decided further “public” meetings were unnecessary. It transpired that Frank Vocci had decided not invite the activists, or send out conference packets to anyone but invited experts.

Cures not Wars huddled, reviewed contacts among libertarian legalizers, and once more initiated the now-familiar drill of phoning, faxing and mailing Ibogaine information to a new group. But this time it was to GOP Congressmen and conservative thinktanks working on de-regulating drug approval. To Cato Institute, the Competitive Enterprise Institute and Gingrich’s own Progress and Freedom Foundation. So the new techno-right was put on notice. Were they interested in a quick techno-fix for addiction?

Only Speaker Gingrich or President Clinton can resolve the current impasse between two committees of Congress and authorize release of $60 million*{*as recommended by the IOM Report} from the Forfeiture Fund (under Criminal Justice) to NIDA Medications (under Health & Environment) for Ibogaine development. Even the biggest advocates of prisons ought to appreciate the fiscal implications of a cure that enables 25-40% of addicts to walk away from addiction without expensive support and social services.

The most interested, though, seemed to be the Cato Institute. [Presumably not directly named after the Roman Cato who declared: “Cartago dalenda est.” …Carthage must be destroyed. To defeat Hannibal. Smash every brick and sow the land with salt, that nothing may grow there, ever again. And pursue Hannibal even to Asia Minor (where he generalled for a while for the Jews), to bring him back to Rome in chains.]

Meanwhile, on Jan 19, 1995, Dhoruba was definitively cleared of the 1971 attack on two NY police officers. The day of Wisdom and the rule of Wisdom had finally come. Manhattan District Attorney Robert Morgenthau, after exhausting every legal manuever to re-instate the original conviction, decided the case was too old to re-try.

A few days later in Rotterdam, after several month of terminal dementia, Nico Adriaans died of AIDS. Despite being an original founder of needle exchange, Nico had somehow become infected, and would be excluded from current Ibogaine trials. That’s unfortunate, because through Ibogaine, he was able to elucidate something very important about addiction and freedom: “If you are resisting suffering, you suffer more. So you know: If you learn from suffering, so that you can know how to act in order to be free, you must accept a lifetime of constant, difficult learning. Addicts stop learning.”

The date of NIDA’s new Ibogaine meeting wasn’t hard to find–March 8. But when David Goldstein requested an invitation, he was informed only designated experts were invited. As an addiction professional who’d been at the previous session in May, Rommell Washington was able to wrangle an invitation on the phone, but no conference packet arrived in the mail.

At this point parallel processes intervened in the person of “Brother Shine” of A.D.A.M., the Afrikan Descendents’ Awareness Movement. Within days of being paroled from a two-year bit upstate stemming from a crack relapse, Thomas Shine was organizing the first broad community forum on Ibogaine in Harlem in conjunction with the Black Coalition on Drugs, inviting among others Deborah Mash and Carlo Contoreggi. For Carlo to come up and speak, approval was needed by NIDA higher-ups.

On February 8, at the regular NIDA Advisory Council*{*held every 3 months} on the campus of the NIH, Dana Beal hand-delivered a letter from the Black Coalition on Drugs to Alan Leshner, asking his approval for Carlo to go to an Ibogaine forum in Harlem, which Leshner gave on the spot. Frank Vocci was there also. He conceded they couldn’t keep the activists out March 8. But because there was only public seating at the Rockville Holliday Inn for ten, it was on a first-come, first-serve basis. Dana said he’d be there at 6:00 AM.

The main preoccupations of the Council session seemed to marijuana, and to a lesser extent finding a cure for cocaine. Leshner reported meeting, in the company of Jim Burke of the Partnership for a Drug-free America, with Bill and Hillary Clinton in the White House. But he wondered aloud why our society has a “unique disconnect” between its understanding of drug abuse as a disease and its drive to punish users. But before the “public comment” at 4:30 PM, Leshner ducked out, leaving his deputy Richard Millstein in charge.

Dana got up and asked whether NIDA was contemplating any public education aimed at keeping the new crop of kids using cannabis from experimenting with the new stronger smokeable heroin under the influence of “grunge” rock, etc. Millstein said the Institute has only two pilot programs, in two cities, aimed at prevent casual users from “graduating.” The attitude that day seemed to be, heroin’s fine–we’ve got methadone.

Now as it happened, neither Deborah or Carlo made it up to the Harlem forum. But Lesher had become aware the Afro-American community was conducting its own review of Ibogaine–a few days before NIDA, on March 4. And Leshner’s office increased seats for the public March 8th to 25 after Kiyoshi Kuromiya called the Director’s office to make sure he had a seat. Then a week-and-a-half before the his forum, Brother Shine invited Leshner himself to come, or send a represenative to Harlem.

Two weeks of intense airplay on WBAI, WLIB, and WRL produced a turn-out of 350 at the Dempsey Center–127 W. 127th, off Malcolm X Blvd.

Brother Shine took the stage, said that as someone born addicted to heroin, Ibogaine was “very personal” to him. He introduced John Morgan, the City College pharmacologist. Professor Morgan recounted the surprise that took hold among skeptical professionals in the field when the work of Glick, Dzoljic, Broderick and others first demonstrated the pharmacological basis in rats–independent of “set and setting”– for Ibogaine’s interruption of addiction.

Howard Lotsof followed with his story of discovery in the ’60’s, development in the ’80’s, and the experience of treating almost 60 addicts in the Netherlands and Panama. Natural healing advocate John Harris spoke on the historical use of Iboga as central to the African Bwiti rite-of-passage involving an entire extended family. Moderator Bernard White of WBAI read a statement on Ibogaine and Re-socialization therapy from Dhoruba Bin Wahad, delayed on a Ghana Air flight. Then Eddie Ellis from Neighborhood Defender made the best speech of the day, placing Ibogaine squarely in the history of Black Panther struggle, COINTELPRO, his own liberation from prison.

Dana wrapped up with the program with word of the NIDA review in Rockville a few days later, inviting everyone to come on down or at least make their views known to NIDA, Lee Brown and Charles Rangel.

On Tuesday, New York state parole officials balked at letting Shine go to Rockville. But a vanload did make it down the next morning to the Crowne Plaza Holiday Inn, a few blocks from NIDA offices at Parklawn. Dhoruba, who came down on his own, brought 6 or 7 local people up from Howard University.

Frank Vocci began promptly at 8:30 AM, saying the question was whether or not it’s safe to proceed in humans.

Rick Strassman presented the Baumann data. It seemed that after denouncing Lotsof’s procedure at the 1987 Ibogaine Conference in Paris (“…Addiction is not in the competence of psychiatry…”), Baumann promptly went home and used the procedure on 35 female addicts, though at about half the dose Lotsof recommends. He also disregarded the contraindication for patients with coronary problems, which apparently cost a life.

Next, Howard Lotsof then summarized about 60 treatments done by NDA International. He offered the first time-lapse video showing Mark LaMontia just before re-treatment, then answering questions of a neurologist at one hour intervals throughout the Ibogaine peak, and then after recovery. The evident pharmacological impact of Ibogaine on the slurred, sideways-glancing, hunched body-language of chronic cocaine/methadone intoxication–the striking transformation of skin and muscle tone–made for a before-and-after comparison no written account can really convey.

Howard characterized Ibogaine efficacy as “15% success, 15% failure, with the length of interruption in everyone else falling somewhere in between on a bell curve.”

Much more detail was provided on the last eight Panama treatments, with Dr. Dan Luciano and Deborah Mash joining Howard to present their observations. Luciano noted Ibogaine was well-tolerated except for early movement-induced nausea and vomiting, with acute transitory cerebellar/vestibular effects, none persistent. EEGs before, during, and after showed no abnormalities of any kind, not even at the moment of the “splitting of the skull.” A distinct interval of cerebellar reset was not possible, via EEG, to detect.

Deborah Mash provided a trove of new details on blood levels and pharmaco-kinetics of Ibogaine and its active metabolite. She identified noribogaine as 12-hydroxy-ibogamine. Miami found the metabolite is active at the mu and delta opiate receptor sites [!], as well as affecting the dopamine and serotonin transporters. Although presumably the same kind “weak” activity seen at the kappa and NMDA receptors, this filled a great deal that was missing when the only thing stopping opiate withdrawal seemed to be some weak kappa receptor activity.

Her slides showed the visualization phase clearly corresponding to a sharp peak in brain levels of the metabolite itself, which may not exit the brain easily and hangs out in there in peak concentrations between 1 and 4 hours.

Howard concluded the treatment team felt the intrusive taking of bloods interfered with the therapeutic Ibogaine effect–and that expectations of efficacy should be scaled down correspondingly.

Charles Gorodetzky next presented complete autopsy reports on the Baumann death and the possible Dutch heroin o.d., plus the case of Nancy, even though Ibogaine was ruled out as cause of her death. It turns out Baumann, in clear defiance of Lotsof’s recommended procedure, had given Ibogaine to a female with not only 80 percent coronary arterial schlerosis and evidence of previous silent heart attack, but opiates in her urine! In the case of Nicola K., heroin overdose just prior to death was still not ruled out, since she had foil and and empty vial and time in the bathroom to smoke what was in the vial. But sky-high bloodlevels of metabolite (but expected levels of Ibogaine) pointed instead to Nicola K. being an extremely slow metabolizer, who succumbed to respiratory collapse when the ‘weak’delta and mu opiate effects of 12-hydroxy-ibogamine were overly prolonged.

Jim Dingell asked if they’d considered whether glucuronidation was the pathway for eliminating Ibogaine, since the glucuronic acid could still have been occupied processing her previous evening’s opiate use in the liver even without great levels of opiate anywhere else. Or was the p450 pathway involved? Without knowing how exactly Ibogaine and noribogaine are excreted, it might be impossible to figure out what happened to Nicola K.

After lunch Peter Hoyle took over, and made it clear right away that he felt the pre-clinical work hadn’t been done to provide a pharmacokinetic, pharmacodynamic model to support a clinical trial design. Mechanism of action was unclear, and receptor-specificity–kappa-opiate, voltage-dependent NA channel, and NMDA interaction–difficult to extrapolate to a clinical setting. Impressive basic research, but study designs hadn’t provided an objective basis for optimal dose-schedule, route, and duration of administration in a clinical trial. Correlation between nonclinical data and target indication were too weak to provide pre-clinical rationale for Ibogaine efficacy. With Ibogaine, rationale for efficacy and clinical benefit depend totally on previous human data. Two tours of duty at the FDA, he knew how tough this made it. Oftentimes clinical benefits are realized without understanding mechanism. Still, in his opinion, Ibogaine wasn’t ready.
Glick, up next, demonstrated conclusively that something measurable was taking place in his rats that could amount to interruption of addiction in humans. But how, for instance, do you measure in rats the craving newly-recovering addicts keep in check via NA meetings?

Dr. Robert Upton presented mathematical analysis of his rat data showing that whereas Ibogaine was converted to metabolite virtually on the first pass through the liver and other organs, systemic clearance of 12-hydroxy-ibogamine tended be saturable–i.e., elimination would be slow at first and then gain momemtum. Ibogaine may even actually be de-methalated by enzymes within the brain, where noribogaine may behave “as if trapped in the brain” due to the different electrical charge on the ibogamine.

With such drugs, the enzymes that clear the drug are overwhelmed until levels fall. With a drug that really saturate the system, like dilantin,*{*common anti-epileptic medication} potentially a 15 percent increment could take effect from marginal to lethal. Although the margin of error with Ibogaine was almost certainly greater,**{**He wanted additonal grants to measure results of low dose Ibogaine over time. He also confided rats don’t have gall bladders, however–a human organ that may be important where gall is concerned.} he urged great care with the dose. Additionally, dose-relatedness is complex–with blood levels showing concave instead convex curves–indicating uneven solubility.

Peter Hoyle came back up. He presented horrendous toxicities, necrosis of organs and fluid in body cavities acheived by overdosing female dogs (50 mg./kg,) continuously for 15 days, or setting new definitions of the lethal dose level in rats by giving 200 to 800 mg./kg. Only one died!

In the hall Curtis Wright intimated that Hoyle had been burned approving AZT, okayed on a showing of efficacy in just 20 persons.

Mark Molliver said glial cell activation in his primates was minor, and the kind of Purkinje cell damage seen in rats so rare that he concluded neurotoxicity is not important in primates. But he saw a syndrome of withdrawal/respiratory slowdown leading to collapse and death–an outcome that could be obviated by massaging the animal to bring it around. And the doses he was using (150 mg./kg. 5 times every 2 1/2 hrs.) caused seizures. Molliver also gave neurotox results in monkeys on 12-hydroxy-ibogamine, which turned out to have “only a fraction” of the toxicity of Ibogaine itself–though in all the same sites, in the Purkinjes of the cerebellar vermis and so-on. It was also strongly hypotonic,* [*ataxic, sleep-inducing] not tremorigenic like Ibogaine. But brain levels reached this extraordinary inverted “V”-shaped peak because noribogaine passed easily into the brain and then couldn’t get out, at least not very fast. What this presented was a new, pharmaco-dynamic picture of the “splitting of skull”: of the 12-hydroxy-ibogamine punching through–and abruptly reversing–the oscillating Ibogaine effect, and then reaching a sharp peak for a few hours in the brain before falling off in line with the ending of the visions. So a distinct interval of cerebellar reset, if any, might lie in this moment of discontinuity between the effects of drug and metabolite, not the transition from normal wakefulness to drug.

Deborah Mash got up and presented neurotox data on her primates, which showed no damage. Then she pulled out her trump card. She pulled out her human brain. Nancy’s brain, which by the greatest coincidence of all, was the perfect specimen for determining faint trace neurotoxicity in human females.

There was evidence of chronic vitamin E depletion caused by drinking on top of methadone; but brain sections failed to show any damage to Purkinjes in the critical area of the cerebellar vermis.

The trend was clear: even though some of the animal toxicities were horrendous, at therapeutic levels Ibogaine is non-neurotoxic in humans, and noribogaine even less so. In animals high doses are toxic–increasingly so as researchers moved from primates to the rat and dog, but only at prolonged exposures, which might be generating distinct toxic metabolites.

When Molliver suggested he would like to tke his own look at Nancy’s cerebellum, though, Mash shot back–“I’ll trade you my brain samples for yuour blood levels.” She felt that Molliver’s primate deaths were particularly senseless, since he hadn’t even bothered to track blood levels of Ibogaine to correlate with the rest of his data.

Next was Juan Sanchez-Ramos with his findings from the stalled Phase I clinical trial. Out in the hall Dhoruba was talking to the ONDCP rep. Barbara Roberts, asking to meet Lee Brown instead of being put off to the end under public comment. Inside, Bonnie Levin explained the battery of neuro-tests to be given to subjects of the Panama treatments. Aside from minor difficulty with re-call in one subject immediately after Ibogaine, she found no cognitive deficits or impairment. Walter Ling presented the draft protocol, and the main modification Grudzinskas suggested was to unblind the blood level data, so that it could be carefully monitored before each dose escalation.

Howard volunteered that NDA now considered Phase I procedures too intrusive; and that they’d rather do a quick, simple safety trial followed by clinical determinations in men focusing exclusively on efficacy against different addictive drugs. He repeated his call for low-dose testing in women, saying it would have to be tackled sooner or later. But when Frank Vocci sounded out the outside consultants, it was clear some of them were still unfamiliar with, or just didn’t believe in, the whole idea of an addiction interrupter.

So it fell to Dana to rebuke them for looking at Ibogaine in a vacuum, when the most important new vector for AIDS is sex-for-crack, according to data from Don DesJarlais published a week earlier in the New York Times*: {*”Maybe as much as half of the new infections among heterosexuals are occuring in relation to crack cocaine…” …HIV is transmitted more easily during two periods: when a person first contracts the virus and a decade or so later when the immune system is collapsing. If a woman…has sex 100 times with a man who is infected…but…latent…she is much less likely to get infected than if she has sex just once with one man who may be…infectious… So a woman is at much greater risk having sex once with 100 partners, most of who are infected.–“New Picture of Who Will Get AIDS is Dominated by Addicts,” by Gina Kolata, New York Times, C 3}
“The reason we’re all sitting here is that there is no known pharmacotherapy for cocaine. If we have to go into humans anyway to find out which other species is most like man, we might as well procede in man. As for dropping efficacy, we were told a showing of efficacy would make-or-break Ibogaine. How big was the sample used to approve AZT? We have 65 Ibogaine treatments. Don’t make us wait another 3 years before going into humans.”

Peter Hoyle, incredibly, argued that second thoughts about AZT justified a double standard for Ibogaine, despite much more clearly established benefit, and some permanent interruptions of addiction with Ibogaine.*{*There has never been a single case of AIDS cured with AZT.} Frank Vocci cautioned the room that this meeting was not designed to come to consensus, and announced an end-of-the-month deadline for outside consultants to file their recommendations and comment. No matter what the outcome, it will be revisited. The irresistable force of a public demanding medicines to stop addiction is up against the immovable object of the experts who believe only maintenance drugs are possible, or even desirable. During the session, Dana released a letter he and Dhoruba faxed Leshner the Day before, which said in part– “… without a much higher profile on the distinct dangers of heroin, your present public relations campaign in conjunction with Jim Burke and the Partnership may well re-enforce the perception that heroin is not that much worse than marijuana–or really that different. Even more than rock scene or celebrity status, this perception that heroin is not really that different from other drugs is an essential ingredient of “heroin chic.” “Inasmuch as NIDA is doing yet another review of Ibogaine’s clinical possiblities, …a small safety/efficacy trial of Ibogaine this year in a few opiate addicts would both provide that media focus and deliver concrete benefits against heroin addiction in the near future. Do something that sends a real message.”

More than one speaker on the 8th, acknowledging growing pressure to go ahead in humans, warned of safety considerations being “swamped” in the rush to use Ibogaine if the first small trial confirms efficacy. According to Carlo, “Even if Ibogaine is slowed down, it’s about three years too late to stop it. They know it works. Even if in the end they can’t use it in people, NIDA views Ibogaine as a fascinating window into the human brain, a probe to the farthest reaches of addictive behavior.”

Frank Vocci, for instance, sees the Ibogaine NMDA receptor activity as a possible clue that “strong memory” in the amygdala–where you lay down long-term memories, as well as remembering what you’re doing from moment to moment–may involve NMDA activity which is as integral to addictive craving as the dopamine activity in the nucleus accumbens ‘pleasure spot.’

The persistence of 12 hydroxy-ibogamine in the brain may also be the key to Ibogaine’s “re-set” of endorphin levels from the chronic deficity of heroin addiction. According to finings of Dzoljic, the weak by long-lived noribogaine effect on all three opiate recptors potentiates production of endogenous nor-harman, the neurotransmitter of eidetic memory and dreams– in effect ‘fooling the system’ because another of the active metabolite’s effects, like nor-harman, is itself to reverse to reverse built-up tolerance, so receptors can tehn signal normal production of endorphins to resume. In fact, Lotsof believes nor-harman is also the body’s first line of defense against opiate addiction, but that without help from the metabolite, it is simply overwhelmed by heroin.

The underlying hypothesis–that the opiate and NMDA receptors are in fact one, interactive receptor-complex–is supported by recently published fings that Ibogaine (but not according to Glick, noribogaine) binds to a site called “sigma-2,” the receptor for haldol. None of the other NMDA receptor drugs like PCP, MK801, or ketamine bind to the sigma receptors, which were first thought to be a fourth opiod-receptor type because of affinity for benzomorphans–then rejected as true opiuod rec ptors because of zero affinity for morphine and naltrexone. But different sigma drugs have been shown to attentuate or potentiate NMDA activity.

In the complex opioid /NMDA receptor interaction, the probable function of sigma-2, especially, is down-modulating hallucinogenic kappa and NMDA effects–just as kappa in turn downregulates primary mu euphoria yet prolongs analgesia, and NMDA activity obviates build-up of tolerance/withdrawal. Interestingly, both NMDA and sigma-2 ligands are considered neuro-protective.

On the other hand, these kinds of “mixed,” agonist/antagonist effects with Ibogaine (tremorgenic, kappa-ergic, with NMDA binding attnuated by sigma-2 activity) raise the interesting possibility that Ibogaine both potentiates and paritailly antagonized the effects of its active offspring noribogaine (hypotonic, serotonergic, weakly active at the mu and delta, as well as kappa and NMDA sites–but not at sigma-2). This is because glutamate and glycine are necessary to “unlock” the NMDA receptor. Therefore NMDA activity and any modulatory sigma-2 effect must entrain with Ibogaine’s rhythmic (10-times-a-second) glutamate firing, driven by the olivo-cerebellum. And during the peack, visualization phase, Ibogaine tremore is shunted into “flickering” back and forth between Ibogaine and noribogaine modes, which subjects experiences as “two world super-imposition”–as the sigma-2 pulse of the more potent Ibogaine momentarily brings them down from their Iboga/serotonin dream [“I had only to open my eyes and I was back in the room”] attentuating the NMDA channel bloccker effect and letting in a nano-pulse of calcium.

Calcium channels/actions potentials are also possibly being modulated by Ibogaine’s kappa effect. But according to Henry Shershen even this kappa effect is definitely mixed, since Ibogaine blocks ordinary kappa inhibition of dopamine, gutamate and locomotor activity. The main effect of Ibogaine pre-treatment was to inhibite serotonin release–and depletion–by cocaine. Dopamine was not inhibited, indeed Ibogaine initially released DA. Instead noribogaine–possibly by sensitizing the serotonin receptor–seems to block dopamine from further run-up.

Not only does this explain how the dopamin in Broderick’s Ibogainized rats goes up only sligtly while the untreated controls goes sky high, but it indicates 1) that multiple receptor interactions control cocaine dopamine release, 2.) that at least three receptor systems are most likely involved in natural recovery. All of which makes NIDA’s opposition to a multi-receptor treatment for coke seem more and more predicated on keeping the distinction between dopminergic and non-dopaminergic drugs from ever becoming clear to the general public.

Adam N., recently re-interviewed, provided the add itional insigt that the process of working the aches out of one’s body for several days after a treatment may be fairly integral to the successful interruption of opiate dependence. Just as some kind of prolonged up-regulation of nor-harman by lingering iboga metabolite my be necessary for the successful “re-set” of endorphin receptors, this upsurge of endorphins cuased by tremor-induced body aches that settle in at the beginning of of the introspective period–following after peaks of Ibogaine and 12 hydroxy-ibogamine–my put opiate addicts on the pharmaco-kinetic equivalewnt of a glide-path to receptor re-set. Indirect evidence of such an effect is seen in the longer recovery times Lotsof notes that heroin and methadone addicts seem to need after Ibogaine, compared to the relative ease with which cocaine abuser recover.

Or put another way, the unease and imbalance addicts experience when their dopamine levels aren’t high enough may be eliminated during Ibogaine as naturally as a boat righting itself in water–via cerebellar/vestibular “re-modeling” of the self flickering between waking space/time and the circuit that allows us, while dreaming, to walk and run even when we’re flat on our back.

On the other hand, if a certain “symmetry” is necessay between this after-surge of natural endorphines and the earlier Ibogaine and noribogaine peaks, then conversely the uncertain pharmaco-kinetics of “dueling peaks” of Ibogaine and its systemically saturable offspring, as well as a review of information on slow wave acitivity and the immune system, might seem to suggest a correlation in two of out three supposedly Ibogaine-related deaths with administration of two distinct does more than a few hours apart (6 and 72 hrs., respectively).

According to Carlo Contoreggi, NIDA now offers vasculitis in the arteries of female dogs that were given 25 mg/kg of Ibogaine for fifteen consecutive days as evidence of toxic build-up of a mtebolite, which according to this theory might have triggered a similar auto-immune response in the death of Nancy, of an intestinal blockage caused by an inflamation of the main artery to the bowels. But careful review of Nancy’s medical history reveals that her intestinal complaint begain the previous summer–well-before her last, double-dose in March of ’94, and four months after her 29-31 mg/kg. does in late March, ’93. And Mash insists that the autopsy showed no vasculitis of the artery in question–only a blooclot caused by a hyper-coagulable state due to a chronic infection in her thigh–leading Nancy Touchette, the only reporter at the March 10th NIDA presentation, to conclude that no really convincing explantion involving Ibogaine alone had been established in any of the three deaths.

Stanley Glick, pursuing the antithetical notion that the interrupter effect is independent of tremor, reports that coronaradine and racimic ibogamine (both non-tremorigenic) interrupt morphine self-administration in rats. Mash, likening noribogaine to a long-acting opiate, told OMNI magazine, “If craving returns to some extent in some people, it may be because Ibogaine’s metabolite are washing out over time. Maybe we’ll need something after Ibogaine for maintainance.” (OMNI, February, 1994, p. 16.)

But if noribogaine and other iboga compounmds are non-competitive NMDA antagonists, like Ibogaine and harmaline, then lthe proper area of inquiry leads into aspects of learing and reorganization of long-term memory that can only be studied in humans. A long-lasting NMDA noncompetitive antagonist metabolite that lingered in the brain might explain the “delayed recall” effect where events from an Ibogaine experience may still snap into focus weeks or even months after a treatment.

Ibogaine’s “acute effect” pharmaco-dynamics, moreover, provide a unique window into the neuro-physics of “two-world super-imposition,” which according to Dick, is to the understanding of Time as particle physics is the understanding of quantum mechanics. According to Einstein, no vision of the future is allowed to get here any faster than speed of light. Simultaneity cannot exist–except that since the reverse of Bell’s theorem has been proven, acording to current particle physics, if a particle is perturbed its anti-matter counterpart is perturbed, simultaneously, even halfway across the solar system. Advanced physics solves this problem by explaining that they are really not separated. Only on an explicate hologramatic level. In implicate reality they are one.

This is reminiscent of Philip Dick’s musings on the Gnostic doctrine of original sin–
“We did not fall because of moral error, we fell because of an intellectual error: that of taking the phenomenal world as real. Therefore we are morally innocent. It is the Empire in its various disguised polyforms which tells us we have sinned… ” (VALIS, pg 97.)

Magical thinking!–but no more magical than the Orthodox miracle of transubstantiation. According to Rome, the wine and the wafer are throughout all Time the body and the blood, which Gnostics call the Plasmate.* So the orthodox are stuck with their own version of Time Travel–but a passive one, without the explanation of a physical mechanisman an ethnopharmacologic basis. By comparison, the idea that these pharmacokinetics have been used at least once before to change history–by receiving information from the future–is relatively strightforward.

Paradoxically, Ibogaine is probably closer than harmaline alone to the interaction of harmala alkaloids plus endogenous neurotransmitters at the moment of crucifixion. So we know Ibogaine can fiddle with time, and alter history. Because it’s been done before. And with its exact mix of opiate and NMDA stimulation, Ibogaine and its metabolite seem to be a lot more effective addressing garden-variety pathologies than harmaline. Ibogaine is going to get a lot of use. Science will not be able to shrink from studying a known example of Time Travel. Time will never be the same again&shyp;
“We are in a maze…which we built and then we fell into and can’t get out…We did it voluntarily; were we such good builders that we could build a maze with a way out but which constantly changed so that, despite the way out, in effect there was no way out for us because the maze&shyp;this world&shyp;was alive? To make the game into something real, into something more than an intellectual exercise, we elected to lose our exceptional faculties, to reduce us an entire level. This, unfortunately, included loss of memory…and here is where we…managed to defeat ourselves, to turn victory over to…the maze we had built&shyp;”(VALIS, pg. 187)

Philip Dick never doubted re-introduction of a Gnostic sacrament would be sufficient, by itself, to free humanity from the maze. Some inkling of the coming Divine Invasion from Africa&shyp;both puritanical Bwiti ethos and the capricious whimsicality of the Ibogaine Coincidence factor&shyp;is captured in the opening lines of Sophia’s VALIS monologue, not included on page 140 of this report:
“…Listen to me; I tell you in truth, in very truth, that the days of the wicked will end and the son of man will sit on the judgement seat. This will come as surely as the sun itself rises. The grim king will strive and lose, despite his cunning; he loses; he lost; he will always lose; and those with him go into the pit of darkness and there they will linger forever.”

Before writing this off as traditionally Christian, obviously derivative from Jewish or Zoroastrian sources, consider the misogynist crank in the beginning of Chapter 12 whose phone-sticker snared the Ibogaine story on the front page of the July 4, ’92 Philadelphia Inquirer. For years, Hank the Skank brooded on this cosmic joke at his expense, while keeping up his crank barrage against 9 Bleecker–and in his phonecranks called it Ib-rogaine, and asked obscenely–“Does ‘Guidi’ do the ‘Wild Thing’?”

A few days after the March meeting, reflecting on the puritan streak in Bwiti, Dana realized what a truly bad idea it was to make dirty jokes about the Ibogaine Coincidence Factor. The next time Hank called Dana told him: “Something really bad is going to happen to you. Very soon you will have incredibly bad luck. Very bad luck. Don’t dis the Bwiti!”

In the wee hours of Monday morning March 20th Capricious Whim struck again. The super at 5901 10th Ave brought in the police to open the door to fix the leak in Apt. 3B. Once inside they found bomb-making materials, nail and incendiary bombs, grenades, 12 rifles (including an AK-47 in plain view), 7 pistols (including a Glock), 10 thousand rounds of ammunition, along with terrorist manuals, “numerous books and magazines about war and Hitler with Nazi emblems on shelves and counter-tops.” Because of the statute of limitations, they couldn’t get the tenant, Henry Neuslein, for the bomb that blew up in the face of the two cops on St. Paddy’s Day 1981. But that morning 16 years of 5:00AM cranks stopped. Sometimes an Act of God only needs a leak, not a flood.

Still, it’s hard to explain something like a Coincidence Factor–especially hard to get the idea across to people who don’t believe Ibogaine works to begin with. On April 6 the FDA gave the University of Miami team a hearing on their request to escalate the does in their safety trial, and took the whole matter–including Nancy’s autopsy, under advisement.

On May 14-16th in Atlanta, Mayor Bill Campbell, Lee Brown, Sue Rusche, and Joe Califano convened the first meeting of a new group, American cities against drugs (ACAD), specifically designed to stem the advance of harm reduction from Europe. Instead they called for “prevention,” the idea of stamping out every single manifestation of drugs with equal fervor–from marijuana decals to bags of smack. Together with the DEA (touting “community policing” as prevention), they had succeeded in reversing the original Clinton pledge to make treatment for “hard-core drug users” the number one drug control priority. After meeting with Partnership Head James Burke and Alan Leshner, Clinton was persuaded toreinstate the Bush/Bennett focus on the marijuana “gateway” as the key to preventing future addiction. Now they proposed to use the mayors to transform their lock on the ONDCP into nationwide ostracism of “legalization talk” from all public debate.

Asked about Ibogaine as a possible “magic bullet,” Sue Rusche told Atlanta Cox radio WGSB that she opposed “swapping a drug for a drug.” On the opening night of the conference Lee Brown deflected a direct question about Ibogaine from Noah Potter, mentioning Landry’s monoclonal antibody and the WIN drug. Minutes later Noah was approached by Lea Palleria Cox, a rep of Otto Moulton’s Concerrn Citizins for Drug Prevention, who told him Ibogaine is “a dangerous, addictive hallucinogen and a fraud,” and that he was “being used.”

At an interactive forum with all the mayors the next day, Noah got to ask them directly about Ibogaine, and the host passed the question off to Herb Kleber, who said dismissively that only a hundred people had taken it, there had been threee deaths, and that it was still in animal studies. But the host (another WGSB reporter) didn’t let it drop there, saying, “All of us are aaginst legalization, butwhere do the mayors stand on AIDS-prevention measures like this Ibogaine, or clean needles to stop the spread of HIV? Everybody’s in favor of clean needles, right?”

Wrong: the Mayor of Worcester, Massachusetts declasre he would never allow it, while Philadelphia Deputy Mayor John Wilder made an impassioned ple to legitimize needle exchange.

On the issue of AIDS, which the ONDCP and NIDA had tried hard the whole time not to mention, the mayors were in total disarray. From the standpoint of the hardliners who’d convened ACAD specifically to torped clean needles, Ibogaine and medical marijuana under the pretext of stopping drug legalization, it was all wrong!

Next to Noah Potter, Lea Palleria Cox groaned and exclaimed, “There goes the conference!” After the mayors were done she got the microphone and addressed them: “You have to understand the countercultue has jumped on the AIDS bandwagon, and they’re using things like legal needles and medical marijuana as wedge issues. That’s why we have to oppose de-crim in any form.”

But another woman got the last word, a conference participant from a small town: “We desperately need treatment. Do any of the mayors have anything to offer us on more availability of treatment any time soon?” No one said a thing. They shuffled their papers.

Alan Leshner did vow in his speech to to ACAD, to “move to a science-based, not ideology-based drug policy by the year 2000.” The next day, back in Maryland, he chaired a meeting that put clinical research into Ibogaine on hold for at least nine months.

Ten days later the FDA reached the opposite conclusion. They aaproved Miami’s protocol, and best all gave Miami their own independent review committee, so they won’t have to keep running back to FDA every time they go up a mg. The bad news is that FDA cut them back from 10 to 8 mg/kg, and somehow they still have to run it by NIDA, even though Leshner says Sanchez-Ramos and Mash have to submit funding requests to regular NIH peer review [just like Don Abram’s marinol vs. smoked marijuana AIDS-wasting study]. MDD funding is totally commited–possibly until after the Miami protocol is complete, in two and a half years–to development of the “WINN cocaine blocker.” No actual target compound exists yet, but computer simulations how that it ought to be possible to design a drug that blocks recognition of cocaine at the dopamine-re-uptake transporter without blocking dopamine binding to the transporter itself.

It will take fifteen years, and hundred of millions in research dollars. But the end result may be a “clean” single-receptor cocaine blocker, which addicts will have to take every day. As Phil Skolnick says, “Existing pharmacological treatments have traditionallly been targeted to specific receptor systems at whgich abused drugs are presumably acting… There are few exception to this receptor-targeting strategy. The use of NMDA antagonists offers a new paradigm… because preclinical data suggest that these compounds are effective in attenuating the development of tolerance and in decreasing the symptoms of dependence on all abused substances.. The recent demonstration Ibogaine is an NMDA antagonist… is consistent with the notion that this class of compounds may offer a general approach to the treatment of addiction.” But even Skolnick distanced himself from Ibogaine a bit, calling for “more specific NMDA antagonists.” In NIDA parlance Ibogaine itself is too “dirty”–acting on too many receptors–even though they were told to expect four distinct anti-addictive effects.

[Ibogasine NMDA activity, according to Mash, is only responsible for down-regulating tolerance: the long-lived metabolite is necessary for the blockade of craving, by elevating serotonin.]

Frank Vocci says that on March 8th, the opponents of Ibogaine were simply stronger in their convictions… that its scientific supporters were too half-hearted. But when the show-down came, every single NIDA clinician was in favor of going ahead. The MDD Phas I/II Ibogaine trial was vetoed by the pharmacologists, the industry reps. The so-called “outside consultants” acted as little more than hired guns brought in to shoot down another Illegal Drug–couldn’t even get their vasculitis theory together with the actual autopsy results. Long-time NIDA grantees who are expert on Ibogaine in human addicts, like Charles Kaplan, were never integrated into the process. MDD never notified the African American treatment professionals who had attended the May 16, ’94 session about the March ’95 conference with the outside consultants. At first, Vocci said there were only ten public seats.

Evidently it will take the entire time until the year 2000 to get to a science-based drug policy. Decision-making at the highest level seems to have been hijacked by pressure groups dead-set against any plan to get at addiction where the main attack doesn’t center on marijuana—even if it involves a cure for addiction itself.

Yet if all it takes to split their consensus into furious controversy is one Ibogaine question, perhaps these people should not be so confident in claiming a monopoly on correctness. After all, many imagine that they speak for God, but as the child Sophia says just after the part about the minions of the Grim King lingering in the Pit–
“What you teach is the word of man. Man is holy, and the true god, the living god, is man himself. You will have no other gods but yourselves; the days in which you believed in other gods end now, they end forever.” (VALIS , pg. 198)

Two thousand years ago, the Annointed One set out to civilize the pagan oppressors who destroyed and sowed cities with salt by enlightening them with the totality of Divine Disclosure.*{*Re-enacting historically ancient Indo-European Myths in order to “download” Torah into Western Civilization} Yet to this day, Western Civilization still reflexively tries to arrest, imprison, and kill its way through problems, instead of finding cures. To treat addiction, our society has opted for repression–drugs that perpetuate addiction–instead of treatments that maximize human autonomy and freedom. Whereas we know He came to free us from sin. Perhaps when enough Junkies take His place–die and are re-born, die and are re-born, each time returning more purified–He will finally be able to climb down off the Cross at last.

Ibogaine represents the next evolution of human life, in the sense that it introduces a new stage of development–the initiation–to the journey from birth to death. Ibogaine enables each person to go forward to the end of their life, see their life flash before their eyes, and come back to live out their life as they would have–if only they had known.

It is as if the Supreme Judge, in the Higher Interest of Justice, established the equivalent of a drug court, granting each person an appeal for extraordinary relief early on–in effect a pre-trial hearing which gives one’s Advocate an additional opportunity to argue on your behalf. But this is also the next stage of spiritual evolution, because it extends the reach of the due process, of the Advocate (Yetzer ha tov) and thereby the Court itself.

The sign and the seal of a Higher Jurisdiction is that afterwards, even the most reluctant addicts tend to concede that life after death is now a fact within their personal experience. They no longer fear it. The feel stronger, more optimistic; they no longer become so exasperated with things.

The miracle is that none of this contravenes any physical law. All of it happened, and happened according to the ordinary workings of nature. There are, of course, many other explanations for all of these things. But no other single explanation so elegantly explains everything. And even if everything else could be accounted for, one anomaly remains.

The Ibogaine works.

“Si Il Mouve.”

Underground use* of Ibogaine to treat addiction in the absence of FDA approval, and to get folks off drugs in defiance of the DEA, is now being reported.

Ibogaine is not going away. This report and appendices have been prepared so that subsequent researchers know where to begin. Et Sepultus resurrexit; certum est quia impossibile est.

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