Emesis or vomiting is a patient condition known to all ibogaine providers. Whether a provider believes there is benefit to vomiting as part of ibogaine therapy or ritual is moot if enough of the drug cannot be absorbed to allow the therapeutic experience. To that end various providers have indicated the use of subtances as diverse as ginger tea, gravol/dramamine (dimenhydrinate), motillium (domperidone) and reglan (metaclopramide). This author participated in research involving all except ginger tea and upon reflection am uncertain if dimenhydrinate or domperidone had any effect above that of keeping the patient motionless. Metaclopramide 20 mg IV was the only medication that immediately stopped vomiting in ibogaine patients. No determination was made of whether oral metaclopramide administered prior to ibogaine would have as significant an effect as the IV administration of the drug. I anticipate this should be determined.
Included herewith, is a report of a dose regimen used to treat a patient who had been receiving 300 mg of methadone per day, the highest dose of methadone dependence yet treated with ibogaine says one provider.
"Something should be said about dose and product," states another author. "First, some new guides, new to the use of ibogaine, may be confused in dose distinctions between HCl and extract. It would be a very unpleasant death, I suppose, with 4 or more grams of ibogaine HCl on board. Second, in my opinion 29 mg/kg of HCl is too much. I experimented with dosages in the range of 13 to 22 mg/kg and came to the following conclusion - 15 mg/kg is for the first time the optimal dose. It is effective for withdrawal and craving and for the vast majority of patients is neither too weak or too strong. Then, from the second treatment on (which I prefer to administer not earlier than 3 or 4 weeks afterwards) the subject can easily cope with 20 mg/kg and does not feel it as stronger than the first treatment."
The proposal of discussion of ibogaine product identity particularly for the benefit of new providers and patients is certainly legitimate as three principal forms of ibogaine of diverse purities are in use in ibogaine therapy. These substances may be, a highly purified form of ibogaine, an extract of T.
iboga, that may be as low as 90% or as high as 99% in purity. Most examples of these products are 95% pure ibogaine. These products are available from commercial chemical manufacturers or by custom manufacturing by qualified chemists in university laboratories. Purified ibogaine may also be obtained by direct conversion from voacangine. This product when available had been assessed at 99.4% purity. The second principal form of ibogaine currently available is a crude total alkaloid extract and contains a reported 15% to 20% total alkaloids of which half is ibogaine. As the other iboga alkaloids contained in the total alkaloid products are active, this material should be viewed as having a potency of 15% to 20% ibogaine equivalency depending on source and batch. These total alkaloid extracts have been supplied by sources in Denmark and Canada. The third form of ibogaine material is the crude plant root bark. Depending on potency, this product may contain from 1% to 6% ibogaine. Most root bark will be in the 2% - 4% range. Any person taking ibogaine or providing ibogaine to another person should be certain of the identity of the substance as confusion of purified ibogaine and a less potent total alkaloid extract might cause a fatal reaction or not be sufficient as a dose to interrupt chemical dependence.
While the initial discovery and early research with ibogaine principally used single doses in the 15 mg/kg - 25 mg/kg range of ibogaine, the expanding base of data being presented by ibogaine providers throughout the world propose multiple dosing regimens. These dose regimens make use of purified ibogaine HCl, total extracts and root bark though principally, ibogaine HCl and total extracts except in the African religious model. Doses considered by a variety of providers to be full therapeutic doses may vary from 15 mg/kg - 25 mg/kg for ibogaine HCl and from 3 gram to 5 grams for total alkaloid extracts for the treatment of chemical dependence. For the purpose of this discussion a full therapeutic dose of ibogaine is one that will precipitate all three stages of ibogaine activity in most but, not all patients: 1) The waking dreamlike state, 2) the cognitive evaluation period and 3) residual stimulation eventually leading to sleep. Depending on circumstance and patient need, full therapeutic doses may be administered in a multidose paradigm a week to months apart.
Adjunct dose levels of ibogaine may be mediate or low. A mediate dose would be 300 mgs to 400 mgs of ibogaine HCl or possibly 1.5 to 2 grams of total extract while low doses may be in the range of 25mg to 50mg total dose range for ibogaine HCl and 100 mgs to 300 mgs of total alkaloid extracts. Mediate doses are generally used to boost a therapeutic dose should opiate withdrawal signs become evident or in the cases of some providers for a broader set of issues. Low dose regimens have been implemented for periods of ten to twenty days after recovery from a full therapeutic dose for antidepressant, antianxiety or antiwithdrawal applications. These regimens have been used in the treatment of both opiate and stimulant disorders in furtherance of the full therapeutic dose of ibogaine. It must be recognized that providing ibogaine is an art and a science and that ibogaine providers will use a multitude of doses individually determined on a patient by patient basis in accordance with the experience of the provider.
For additional information, comparative dose and strength tables from the chapter by James and Renate Fernandez found in Vol. 56 of The Alkaloids series published by Academic Press (2001) are shown below.
| Ibogaine dose to facilitate personal growth and change: | 10 mg/kg |
| Ibogaine single dose in self-help network for addiction interruption: | 20 mg/kg |
Animal studies for neurotoxicity:
|
| Alternate daily dose ibogaine over 60 days [no toxicity]: | 10 mg/kg |
| Ibogaine dose associated with no evidence of toxicity [but decrease in drug self administration: | 40 mg/kg |
| Ibogaine dose associated with cerebellar damage: | 100 mg/kg |
Lotsof
(personal communication in preparation for ibogaine conference)
|
| Ibogaine dose causing modest psychoactivity with euphoria, altered perception of time: | 90-120 mg |
| Amount of ibogaine ingested by adept that would allow remaining centered enough to assist in initiation ritual: | 200 to 300 mg |
| Ratio of fresh root scraping to dry root bark: | 15/1 |
| Proportion of iboga alkaloids in dry root bark (50% ibogaine): | 2 to 3% |
| Rounded teaspoon of root bark: | 3 to 4 g |
| Amount iboga alkaloids in rounded teaspoon per above calculations: | 60 to 120 mg |
| Pick-up dose , iboga alkaloid content of 1 rounded teaspoon of dry root bark: | 60 to 120 mg |
| Large dose for initiation into Bwiti, gradual intake of fresh root scrapings, maximal dose observed: | 1000 g [one kilo] |
| Dose recalculated as dry scraping [1000/15]: | 67 g |
| Content of iboga alkaloids of the above quantity of root scraping, assuming an average 2.5% iboga alkaloid content: | 1.675 g |
| Total maximal Bwiti iboga alkaloid dose calculated per kilo of body weighty in small initiate weighing 50 kilos [hence a high estimate]: | 33.5 mg/kg |
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POST IBOGAINE THERAPY
There is no clarity that any form of adjunct therapy administered during the post ibogaine period following acute ibogaine effects is more efficacious than any other form of adjunct therapy in prolonging periods of abstinence and freedom from drug craving. This is also in keeping with the findings in chemical dependence treatment of non-ibogaine patients. It is the hope of the authors that findings of significance concerning efficacy or advantages of one form of therapeutic modality over another may be addressed in future revisions of the manual. Provider contributions are encouraged.
One author indicates, as for post-ibogaine therapy we have found that it is essential for addicts to quit smoking tobacco. Nicotine has proven to act on receptors that cocaine and other drugs also effect. Statistics show that 90% of addicts smoke and nicotine can cause craving for other drugs. Many patients find that cigarettes taste different after ibogaine and we encourage them to quit by using nicotine patches and Wellbutrin (bupropion HCl).
A second author adds, "With regard to the question of suitable post-ibogaine therapy, my opinion, from personal experience and reading Bwiti literature, is that bio-energetics or other body-based psychotherapies are most useful. The Bwiti dance constantly on iboga in the regular group sessions at the temple (not during the high dose "initiatory" session, you can't move as I'm sure you're aware!) and I'm sure this is for a reason."
"My personal opinion, based on my experience of doing ibogaine, doing quite a bit of therapy afterward, and observing others who've done ibogaine with or without therapy afterward, is that there is sometimes a real problem with integrating the ibogaine experience properly and not simply at an ego-level. The tendency towards developing a 'need' for alternative belief systems to avoid bodily integration of the experience is, in my opinion, particularly marked in ibogaine users. (ie the individual NEEDS to believe something is true as opposed to being able to simply take or leave an idea)"
"Therefore body-based and emotional release therapies like primal, bio-energetics and encounter are probably highly synergistic with the ibogaine experience, in my opinion. My personal recommendation would be Humaniversity therapy, available at the Humaniversity up on the Dutch coast, and available to addicts as the Residential Addiction Foundation Program (RAF Program) lasting 3-6 months or longer."
Another author adds, "I constantly emphasize that to take full advantage of a session it is imperative to follow through with therapy. If the 12 step programs appeal to a person then, by all means incorporate the meetings into the post session program. A couple of ingredients apply specifically to people compelled to consume drugs. One, is they do not want to experience any level of pain, i.e. physical, emotional pain is to be avoided at any cost. The second insight is that a percentage somewhere in the 90's have experienced a deep level of physical and/or emotional abandonment from the same sex parent. Individual therapy, which necessitates finding a same sex therapist to establish the therapeutic relationship which includes transference of initial role model issues within the framework of the relationship is most healing so that by the time the metabolite washes out of the receptors from the session, the deep issues which created the addiction to begin with from the role model relationship in question has solidly begun to be actively addressed. This crucial type of therapy is, to say the least a challenge to create because of the threat it imposes to the very core ego structure. And so in the name of therapy most people will find a counselor who they are comfortable with and not at all intimidated by. This type of talk therapy will not be sufficient."
A fifth author comments, "It's frequent that addicted clients think that if they still feel some withdrawal effects or craving after more than 20 hours after ibogaine intake, then it didn't work out for them and they tend to search for a dose of their drug of choice. The treatment provider must be aware that ibogaine often needs some days to stabilize its effects and therefore should heighten his immunity toward the addict's heartbreaking performances."
"It is important to understand the differences between treating addiction as only a physiological medical condition and treating addiction with its related psychological and social issues. In spite of the fact that ibogaine is not far from being a miraculous treatment tool, the way it is generally used is highly ineffective and wastes ibogaine's potential. I am talking about overnight treatments that do not include an integrated treatment program. Ibogaine simply needs to be incorporated into already existing addiction treatment networks and then it will show its real potential. "
And, a sixth author: "Private therapy is somewhat hit and miss. There are brilliant practitioners out there but not many with any ibogaine experience (if any)." "... bodywork is extremely important." "So for people that are disillusioned by therapists and group counsellors various forms of bodywork can be extremely effective - acupuncture, rolfing, breathwork (rebirthing or Grofs), dance and movement therapy. Anything that reconnects you with the trauma lodged deep in your body. If you have been addicted for years the ibogaine may bring the reasons for the distress to the surface but that won't necessarily release them - especially if they are lodged deep - which is why the previously mentioned practices help."
"I would also suggest that a support group is extremely beneficial. Unfortunately no matter how much I tried I couldn't get the people that I had seen to form an ibogaine support group and I think this would really help. I have seen it help on the ibogaine list. People able to talk to each other about their experiences on line. Perhaps this is the only way to do it but it would be good for example to have a group... that met once a month to talk about things."
"To conclude, no three day recovery program in itself can correct years of substance abuse. It is therefore essential to arrange follow up care. The ibogaine experience itself leaves you open and enthusiastic about creating changes in your life. Post treatment bodywork/counselling is essential, as it will help maintain this positive transformation and facilitate a deeper understanding and release of years of abuse."
While still another reflects, "I think it is important we not only reach for the most significant endpoint in offering ibogaine therapy but, view what we are doing from a harm reduction perspective and a pro-patient perspective in that anything that benefits the patients, short or long-term, should be viewed as a valuable outcome. I think it is universally accepted that multiple ibogaine treatments over time provide better results in most cases than a single administration. This is not to say that a single administration is not dramatic in its ability to interrupt an out of control addiction syndrome. I think it would be fortunate if ibogaine were a legally available medication through both social and private medical insurance programs. Availability coupled with normalization of addiction into mainstream medical treatment will offer the best outcome in our society which is medically directed. Under other circumstance, a religion would do just as well, and that is not to exclude the self-help group or association concept. From what I see of the suggestions of many of the authors, a belief system and the ability to take some action, to allow a sense of power and accomplishment are important."
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Invitation to Contribute
Many questions for which we seek answers remain: How do ibogaine providers best care for ibogaine patients? The primary authors continue to seek a consensus from ibogaine providers and patients as well as, others working in addiction medicine. Is a consensus possible? That remains to be seen but, with each revision of the manual we may come closer.
Submissions should be made to Howard Lotsof. Accepted work will be incorporated into the next revision of this manual and the authors indicated as contributing authors to this manual or not, at their discretion. Revisions shall be made periodically.
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APPENDICES
***********
NIDA DRAFT PROTOCOL
Rising Dose Tolerance Study using Single Administration to Assess Safety and Preliminary Efficacy of Ibogaine for the Treatment of Cocaine and/or Heroin Dependency
Developed/Issued
by
MDD/NIDA
(10/19/93)
Introduction Safety and Exclusion Criteria
Preclinical Studies
Exclusion Criteria
Psychological Assessments
Neurological Assessments
Opioid Withdrawal Assessments
General Physical Condition
Assessments During Treatment
Safety and Exclusion Criteria
[ introductory statements ]
To date, there is no published data from a controlled clinical trial that has assessed the safety of ibogaine in the treatment of drug addictions. Information from the anecdotal reports indicates there is a mild transient increase in blood pressure and a minimal effect on pulse and respiration.
To date, there is no published data from a controlled clinical trial that was conducted to assess the preliminary efficacy of ibogaine in the treatment of drug addictions. The initial observations of effects of ibogaine was a narrative account (L.A.C., 1991) of the results of taking ibogaine in the mid 1960s by seven heroin addicts, five of whom several days later reported no signs of withdrawal, abstinence, and no desire to take heroin.
Of the 7 clients in the mid-sixties, 6 received one treatment of ibogaine and the effects were that 2 resumed heroin use 24 hours later, one resumed heron use 5.5 months later and the remaining 3 were drug-free 6 months after receiving ibogaine. One subject reported receiving ibogaine 5 times and reported abstinence from: heroin use for 3 years, cocaine use for 18 months and amphetamine use for 6 months.
Of the 18 clients in a contemporary group, 17 received one treatment of ibogaine and one received 2 treatments. After ibogaine, two clients continued to take heroin and one resumed heroin use 5 days later. Six subjects were drug-free from 2 weeks to 18 months, but contact was lost with them. Two subjects were heroin-free for six months and were awaiting retreatment with ibogaine. One subject was cocaine-free for 3.5 years. The remaining 5 subjects were drug-free for 2-10 months.
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Preclinical Studies on Ibogaine
Safety Issues
The most salient safety issue is contained in the findings of (O'Hearn et al., 1993) that when rats were administered high doses of ibogaine (100 mg/kg i.p.) glial cells in the cerebellum were activated, thereby suggestive of neuronal damage which the authors hypothesized were most likely the purkinje cells. [see additional documents #1 and #2]
Other safety issues about the effects of ibogaine are contained in the reports of: increased blood pressure and heart rate in conscious dogs and decreased blood pressure and pulse rate in anaesthetized dogs (Gershon and Lang, 1962), decreased blood glucose (ibogaine 20 mg/kg or 40 mg/kg) and increased blood glucose with higher doses in rats (Dhahir, 1971).
Safety Measures - Cerebellar Functioning
Prior preclinical studies indicated that the major safety issue with the administration of ibogaine is the remote possibility of lasting damage to the cerebellum, especially the purkinje cells. The repeated neurological assessments of cerebellar functioning in our subjects will consist of an extensive neurological examination that assesses most of the readily measurable dimensions of cerebellar functioning. The neurological examination was adapted from the application of comprehensive preclinical work on the cerebellum that was summarized in a book by (Ito, 1984) to contemporary texts on neurological examinations (Kaufman, 1990; Scheinberg, 1981). The major neurological signs that indicate cerebellar damage are: dysmetria (inaccurate targeting of goal-directed behavior), delayed movement initiation and delayed reaction time, dysdiadochkinesia (inability to perform rapidly alternating repetitive tasks), hypotonia (reduced muscle tone), disturbances in gait and station, and intention tremor. The check-list for the Neurological Assessment Battery will consist of 12 behaviors that will be evaluated by the following discrete categories of impairment: none, mild, moderate and severe. In addition, while on inpatient status, PET scans will be conducted during the inpatient phase 3 days before and 3 days after the Ibogaine session and during the one-year follow-up assessment battery.
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Exclusion Criteria
1. Patients with a history of active neurological or psychiatric disorders, such as cerebellar dysfunction, psychosis, bipolar illness, major depression, organic brain disease or dementia, that require treatment or that would make study compliance difficult.
2. Patients who have a Beck Depression Inventory score greater than or equal to twenty-four.
3. Patients requiring concomitant medications that may interfere with a clinical trial or evaluation (e.g., anti-epileptic drugs, sedatives, hypnotics, antidepressants, neuroleptics, methadone, meperidine, etc.) [A significant number of patients treated in the last decade outside of this proposed research study have been dependent on methadone, meperidine or sedatives].
4. Patients with a history of sensitivity or adverse reactions to the treatment medication.
5. Patients with a history of significant heart disease or a history of myocardial infarction.
6. Patients with blood pressure above 170 mm Hg systolic/105 mm Hg diastolic or below 80 mm Hg systolic/60 mm Hg diastolic or a pulse greater than 120 beats per minute or less than 50 beats per minute.
7. Patients who have a history of hypertension uncontrolled by conventional medical therapy.
8. Patients who have received any investigational drug within 6 months prior to entering the study. [The authors received a report of concurrent use of ibogaine and 5 methoxy di isopropyl tryptamine (5meo dipt) that precipitated a medical event of near fatal proportions requiring over a week of hospitalization. Additionally the patient was diabetic and did not monitor blood glucose levels.]
9. Patients who have received any drug known to have a well-defined potential for toxicity to a major organ system within the month prior to entering the study.
10. Patients who have clinically significant laboratory values outside the limits thus specified by the investigators laboratories.
11. Patients who have any disease of the gastrointestinal system liver or kidneys, or abnormal condition which compromises a function of these systems and could result in a possibility of altered metabolism or excretion of the study medication will be excluded. As it is not possible to enumerate the many conditions that might impair absorption, metabolism or excretion, the investigator should be guided by evidence such as:
A. History of major gastrointestinal tract surgery (e.g., gastrectomy, gastrostomy, bowel resections., etc.) or a history or diagnosis of an active peptic ulcer or chronic disease of the gastrointestinal tract, (e.g. ulcerative colitis, regional enteritis, Crohn's disease* or gastrointestinal bleeding).
B. Indication of impaired liver function.
C. Indication of impaired renal function.
12. Patients who test positive for HIV virus.
13. Patients with active tuberculosis.
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Psychological Assessments
1. Interviews
A. Addiction Severity Index (ASI)
B. Diagnostic Interview Scale (DIS)
2. Questionnaires
A. Visual Analogue Scale cocaine craving (VAS)
B. Beck Depression Inventory (BDI)
C. Minnesota Multiphasic Personality Inventory-2 (MMPI-2)*
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Neurological Assessments
1. Electroencephalography (EEG)
2. Neurological Assessment Battery
A. Coordination/tremor
a. Finger-to-nose
b. Finger-to-finger
c. Heel-to-shin
B. Coordination/tremor, Repeated rapid alteration tests
a. Palm/back hand slap knee
b. Prone/supine forearm
C. Coordination /ataxia
a. Heel-to-toe walking
b. Romberg test (feet together, eyes open/eyes closed)
D. Muscle tone/hypertonia
a. Resistance to stretch
E. Reflexes
a. Acoustical startle
b. Pupilary light reflex
c. Vestibulo-occular reflex
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Opioid Withdrawal Assessments*
1. Objective Opiate Withdrawal Scale (OOWS)*
2. Subjective Opiate Withdrawal Scale (SOWS)*
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General Physical Condition
1. History and Physical
2. Electrocardiogram (EKG)
3. Laboratory
Blood Work
a. CBC DIFF
b. AST ALT
c. Hepatitis screen
d. Thyroid panel
e. SMA-18 profile
f. CHEM-25
Urine
a. Routine urine analysis
b. Toxicology screen (positive for target drugs)
1. cocaine
2. morphine (heroin)
3. cocaine
4. ibogaine
Dermal Tuberculin (if positive or previously immunized, then chest x-ray)
Breathalyzer
Vital signs with weight
HIV test and counseling
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Support staff and design of environment
Generally, the session room should be pleasant and the social interactions with staff members supportive. Pastel-colored walls, comfortable hospital bed, soothing murals, paintings or pictures, a comfortable chair for the staff member or therapist to constantly observe the subject during the ibogaine experience. Dim lighting and quite setting. Dialogue should be initiated by the patient. Reduce the need for walking by having a patient lavatory nearby.
Within this context, allow the patient to sleep and rest peacefully ad lib. Otherwise, when the patient is in the talkative phase, the staff member should attentively and unobtrusively attend to but not initiate conversation.
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Assessments [during treatment]
Cardiovascular - Apply ambulatory pulse and blood pressure apparatus that is programmed to obtain and record digital quantities q 30 min for a 24 h period. Apply device just before dosing.
Neurological - Observe for the onset (that is time from the administration of ibogaine) for drug-related changes in neurological functioning (e.g., the onset of changes in speech patterns, nausea and vomiting)
Psychological - Observe and record what patients spontaneously say, Record the onset and duration of the somnolent phase.
Related Protocol Bibliography
Dhahir. A comparative study of the toxicology of ibogaine and serotonin. Doctoral Thesis. 1971. return to chapter
Gershon S., Lang W.J., A psycho-pharmacological study of some indole alkaloids. Arc. Int. Phamacodyn. 85, 31-62, 1962. return to chapter
Ito, M. The cerebellum and neural control. New York: Raven Press, 1984, Pp. 353-465. return to chapter
Kaufman, D.M. Clinical neurology for psychiatrists (3rd Ed.). Philadelphia: W.B. Sanders Co., Pp 18-20, 1990. return to chapter
L.A.C. Can a psychedelic drug cure drug addiction? The ibogaine story. Drugs, Toxic Chemicals and Health 6, 1-2, 1991. return to chapter
O'Hearn E., Long D.B., Molliver M.E. Ibogaine induces glial activation in parasagittal zones of the cerebellum. Neruroreport. 4, 299-302, 1993. return to chapter
Scheinberg P. Modern practical neurology; An introduction to diagnosis and management in common neurologic disorders (2nd Ed). New York: Raven Press 1981. return to chapter
***End NIDA Protocol Selections***
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Additional Documents
1. An evaluation of ibogaine neurotoxicity, including abstracts of relevant papers. Return to chapter
2. Daniel Luciano MD describes neurological observations of treatment with ibogaine. Return to chapter
3. What's in a
blood test? (SMA-20). You are about to find out.
Return to chapter
4. A good place to learn the terms used in blood test reports, their meaning and the significance to health related issues. Return to chapter
5. A CBC or complete blood count along with a differential that indicates the breakdown in the types of white blood cells offers a comprehensive view of blood chemistry in conjunction with the SMA-20. Return to chapter
6. A general review of cardiovascular disorders can be found at The Open Directory Project and at The Medical Center Online. The topic is also well covered in Section 16 of the Merck Manual Return to chapter
7. Everything you want to know about electrocardiograms if you could think of the questions. Return to chapter
8. This early report, Reflections on an Ibogaine Experience, provides an excellent treatment overview that includes concurrent ibogaine/heroin use by the patient. The survival of this patient should not be taken to indicate the survival of other patients under similar circumstance. Return to chapter
9. A copy of the Beck Depression Inventory is available as an FDA document. This page automatically downloads the pdf file of the beck depression inventory to your computer. PDF files require adobe reader programs that are available at no cost from Adobe return to chapter
10. The Minnesota Multiphasic Personality Inventory MMPI-2 may prove a valuable tool in assessing pre and post-treatment behavior of patients. Return to chapter
11. The Diagnostic and Statistical Manual of Mental Disorders, 4th. Edition, better known as the
DSM IV, offers detailed descriptions of broad ranging psychiatric disorders.
Return to chapter
12. Treatment of Acute Opioid Withdrawal with Ibogaine. Alper et al.'s review article of ibogaine effects on opioid withdrawal signs of subjects from the United States, The Netherlands and Panama over a period of three decades is now available as a downloadable PDF file. In order to read a PDF file you will require an adobe reader program from Adobe. Return to chapter
13. The early paper (1995) Ibogaine in the Treatment of Narcotic Withdrawal by Lotsof, Della Sera and Kaplan provides useful information on the comparative effects of ibogaine and narcotic withdrawal. Return to chapter
14. Ibogaine in the Treatment of Chemical Dependence Disorders: Clinical Perspectives offers an overall view of ibogaine therapy and what may be anticipated during treatment. Return to chapter
15. Frenken, an early ibogaine researcher provides her views on ibogaine therapy in An Ibogaine Treatment Protocol providing a view of the Dutch ibogaine self-help movement. Return to chapter
16. Nick Sandberg presents a thorough review of ibogaine safety, effects and history in his original work Introduction to Ibogaine return to chapter
17. A good place to begin to gain an understanding of a structured report form. Guidelines for psychiatric evaluations of Adults. return to chapter
18. Catalogue of diagnostic questionnaries. return to chapter
19. Brief Psychiatric Rating Scale. return to chapter
20. The Sexual Inequality of Drug Metabolism. The Scientist 16[6]:29. return to chapter
21. Notes to Treatment Providers by H. Wells gives a view of ibogaine treatment issues in the United Kingdom. return to chapter
22. Always of value, a medical encyclopedia. return to chapter
23. "Merck & Co., Inc., is proud to introduce The Merck Manual of Medical Information--Home Edition.. This all-new publication is based on The Merck Manual of Diagnosis and Therapy, Centennial Edition , commonly referred to as The Merck Manual, the textbook of medicine most widely used by health care professionals in the U.S. and worldwide. The Home Edition transforms the language of the professionals' version into commonly used English while retaining the vital information about diseases, diagnosis, prevention, and treatment." The reader should review both volumes to determine which best meets your needs. "The Merck Manual of Medical Information--Home Edition, like all the Merck manuals and The Merck Index, is published by Merck & Co., Inc., on a not-for-profit basis. Copyright © 1995-2001 Merck & Co., Inc., Whitehouse Station, NJ, USA. All rights reserved." return to chapter
24. How to Safely Use Ibogaine, a public document of the Iboga Foundation, a not-for-profit group in Slovenia approaching ibogaine use from a religious perspective.
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The figure above depicts how serotonin neurotransmission may be modified at the presynaptic level by inhibiting degradation, storage or reuptake.
