First Appearance
How is Ibogaine treatment different from any other form of addiction treatment? It is an ADDICTION INTERRUPTOR; it permanently eliminates addiction and cravings and resets the brain to its pre addiction state. Ibogaine was first marketed to the public in France and was sold as a medical stimulant in the 1930s. Sold in 8mg tablets in the form of Lambarène, it was advertised as both a mental and a physical stimulant. It showed “greater than normal efforts” by healthy individuals and also was used to help treat depression. After World War II, Lambarène became popular amongst many veteran athletes but was removed from the market after its ban in 1966.
Ibogaine counteracts a person’s addictions through powerful disruptive effects on the brain and addictive behavior. It causes them to regain control of their lives by effecting at least three types of major brain receptors.
Researchers have made some interesting findings. It is known that Ibogaine and Noribogaine bond with Opioid receptors, the same receptors that opiates like Heroin and Morphine bond with. It also seems to ease the transmission of information along Opioid addiction. It bonds with the same receptors as Opiates while improving the function of Opioid Neurotransmitters. In doing so, It prevents withdrawals, while the Opiates flush out of the system. It prevents cravings from re-emerging.
Essentially, Ibogaine hits a reset button. You come back down fundamentally rearranged. Things are not the same; there is an entire spectrum of changes taking place, It brings your body and mental health back to a pre-addiction state. Anecdotal reports show immediate reduction in drug cravings, no withdrawal symptoms, and greater self-control.
What is Ibogaine? – A Complete Overview of Ibogaine
Ibogaine is a natural extract from the plants in the Apocynaceae family. It includes such plants as the Tabernanthe Iboga, Voacanga africana and Tabernaemontana undulata, and is native to West-Central Africa.
Everyone who has taken Ibogaine reports that the session is the most intense experience of their life. At the same time, however, It is very gentle. It will not overwhelm you, nor cause any harmful side effects.
Ibogaine was first marketed to the public in France and was sold as a medical stimulant in the 1930s. Sold in 8mg tablets in the form of Lambarène, it was advertised as both a mental and a physical stimulant.
It showed “greater than normal efforts” by healthy individuals and also was used to help treat depression. After World War II, Lambarène became popular amongst many veteran athletes but was removed from the market after its ban in 1966.
Ibogaine and Parkinson’s
The following is a summary on existing research looking at the influence of Ibogaine on glial cell line-derived neurotrophic factor (GDNF) levels in the brain, and the beneficial impact that an increase in this protein can have. Ibogaine stimulates the glial cells to produce more dopamine. Existing studies have examined these areas, and have identified a direct link between Ibogaine, GDNF expression and neurodegenerative diseases. Glial cell line-derived neurotrophic factor (GDNF) is a disulfide-linked, homodimeric protein that promotes the survival and morphological differentiation of midbrain dopamine neurons .The ability of GDNF to act as a growth factor for dopamine neurons makes Ibogaine the most valuable treatment for Parkinson’s Disease (PD), a debilitating neurodegenerative disorder caused by a loss of dopamine neurons in the substantia nigra. The loss of dopaminergic neurons in PD leads to deficient levels of dopamine in the striatum and subsequent dysregulation of motor control. Following is a presentation examining the biochemical background of Ibogaine and GDNF in more detail. Glial cell line-derived neurotrophic factor (GDNF) is a disulfide-linked, homodimeric protein that promotes the survival and morphological differentiation of midbrain dopamine neurons. The ability of GDNF to act as a growth factor for dopamine neurons make it could be a valuable treatment for Parkinson’s Disease (PD), a debilitating neurodegenerative disorder caused by a loss of dopamine neurons in the substantia nigra. (6). The loss of dopaminergic neurons in PD leads to deficient levels of dopamine in the striatum and subsequent dysregulation of motor con
One reason Ibogaine is so interesting is that it increases levels of glial cell line-derived neurotrophic factor (GDNF) in the brain (He & Ron 2006), and this in turn appears to be a potent survival factor for several different neuronal populations in different brain regions (Boscia et al. 2009) and has neuroprotective properties that promote the survival of both dopaminergic and motor neurons (Bermingham et al. 2004; He and Ron 2006), which may be one of the reasons for the prolonged afterglow often experienced following treatment with the drug. Furthermore, GDNF can cause sprouting of dopaminergic fibers and clinical improvement in experimental animal models of Parkinson’s disease, as well as a similar sprouting of dopaminergic fibers in humans with the disease, with the resultant clinical improvement in symptoms (Love et al. 2005). GDNF has also been identified as having anti-addictive properties (Ron & Janak 2005; Carnicella & Ron 2008.) This may be one of the reasons for Ibogaines’ effectiveness in treating drug addicts with impaired receptor function, but this drug is also a considerable ally to those with degenerative neurological diseases.
Both Parkinson’s disease and Motor neuron disease are chronic disorders with no known cure, and require management with drugs that can have considerable side effects, causing a very poor quality of life for terminal stage sufferers of these diseases. By contrast, a low dose regime of Ibogaine or Iboga alkaloid extract would be of low toxicity and free of serious side effects.
GDNF has been shown to have a potent neurotrophic factor in both rodent and primate as well as human models of Parkinson’s disease (Gill et al. 2003). Direct brain infusion of GDNF into the brains of five Parkinson sufferers resulted in a 79% improvement in the off-medication motor subscore of the Unite Parkinson’s Disease Rating Scale (UPDRS) and a 91% improvement in the activities of daily living subscore (Gill et al. 2003). Positron emission tomography (PET) scans of dopamine uptake showed a significant 68% increase in putamen dopamine storage after 18 months, indicating a direct effect of GDNF on dopamine function. Furthermore, after one year, no serious clinical side effects were observed (Gill et al. 2003). The use of Iboga alkaloid extract of Ibogaine provides a longer term and much less invasive method of GDNF administration than direct brain infusion.
Regarding motor neuron disease, the research that has occurred in this area, such as gene transfer of neurotrophic factors, suggests great success potential in the treatment of motor neuron disease (Haase et al. 1997). Again, Ibogaine therapy may offers a straightforward, non-invasive, inexpensive, low-toxicity method of treatment for sufferers of this disease.
Thus based on this previous research, it is clear that with Ibogaine, GDNF expression and neurodegenerative diseases is certainly warranted, despite the financial and political hurdles of working with Ibogaine, a largely scheduled yet natural alkaloid extract from the root bark of the West African shrub Iboga (Tabernanthe iboga). The drug is of little financial interest to pharmaceutical companies, and quite inaccurately deemed to be of “no medical value”. Legal red tape is less restrictive for Ibogaine in Europe and Mexico than it is in many other parts of the world.
Bermingham, N., Hillermann, R., Gilmour, F., Martin, J. E. and Fisher, E. M. C. (2004) Human glial cell line-derived neurotrophic factor (GDNF) maps to chromosome 5. Human Genetics, 96, (6), 671-673.
Boscia F, Esposito CL, Di Crisci A, de Franciscis V, Annunziato L, et al. (2009) GDNF Selectively Induces Microglial Activation and Neuronal Survival in CA1/CA3 Hippocampal Regions Exposed to NMDA Insult through Ret/ERK Signalling. PLoS ONE 4, 8, e6486. doi:10.1371/journal.pone.0006486
Carnicella, s. & Ron, D. 2008. GDNF – A potential target to treat addiction. Pharmacology & Therapeutics, 122, (1), 9-18.
Gill, S. S., Patel, N. K., Hotton, G. R., O’Sullivan, McCarter, R., Bunnage, M., Brooks, D. J., Svendsen, C. N. and Heywood, P. (2003) Direct brain infusion of glial cell-line derived neurotrophic factor in Parkinson disease. Nature Medicine, 9, 589-595.
Grondin, R., and D. M. Gash. 1998. Glial cell line-derived neurotrophic factor (GDNF): a drug candidate for the treatment of Parkinson’s disease. Journal Of Neurology 245, 35-42.
Haase, G., Kennel, B., Pettmann, B., Vigne, E., Akil, S., Revah, F., Schmalbruch, H. and Kahn, A. (1997) Gene therapy of murine motor neuron disease using adenoviral vectors for neurotrophic factors. Nature Medicine, 3, 429-436.
He, D. Y. & Ron, D. (2006) Autoregulation of glial cell line-derived neurotrophic factor expression: implications for the long-lasting actions of the anti-addiction drug, Ibogaine. The FASEB Journal, 20, 2420-2422.
Kirik, D., B. Georgievska, and A. Bjorklund. (2004) Localized striatal delivery of GDNF as a treatment for Parkinson disease. Nature Neuroscience 7:105-110.
Love, S., P. Plaha, N. K. Patel, G. R. Hotton, D. J. Brooks, and Gill, S. S. (2005) Glial cell line-derived neurotrophic factor induces neuronal sprouting in human brain. Nature Medicine 11:703-704.
Ron, D. & Janak, P. H. (2005) GDNF and addiction. Reviews in the Neurosciences, 16, (4), 277-285.
A patent application was filed in 2005 for treating and preventing neurodegenerative disorders such as Parkinson’s, Alzheimer’s disease, dementia and mild cognitive impairment with ibogaine.
Ibogaine increases levels of glial cell line-derived neurotrophic factor (GDNF) in the brain (He & Ron 2006), and this appears to have neuroprotective properties that promote the survival of both dopaminergic and motor neurons (Bermingham et al. 2004; He and Ron 2006). GDNF can also cause sprouting of dopaminergic fibers and clinical improvement in experimental animal and human studies in which the test subjects had Parkinson’s Disease, with the resultant clinical improvement in symptoms (Love et al. 2005). GDNF has been shown to have potent neurotrophic factor in both rodent and primate models of Parkinson’s disease (Gill et al. 2003). Direct brain infusion of GDNF into the brains of five Parkinson sufferers resulted in a 39% improvement in the off-medication motor sub-score of the Unite Parkinson’s Disease Rating Scale (UPDRS) and a 61% improvement in the activities of daily living subscore (Gill et al. 2003). Positron emission tomography (PET) scans of dopamine uptake showed a significant 89% increase in putamen dopamine storage after 18 months, indicating a direct effect of GDNF on dopamine function. Furthermore, after one year, no serious clinical side effects were observed (Gill et al. 2003).
Both Parkinson’s disease, motor neuron disease and Alzheimer’s Disease are chronic disorders with no known cure. Most neurodegenerative diseases require management with prescription medications that can have considerable side effects, which may cause a very poor quality of life for terminal sufferers. In turn, Ibogaine may be very beneficial to those with degenerative neurological diseases.
The use of Iboga alkaloid extract or Ibogaine would provide a longer term and much less invasive method of GDNF administration than direct brain infusion. Thus, further research on Ibogaine and GDNF is certainly warranted. Ibogaine therapy may offer a non-invasive and low-toxicity method of treatment for sufferers of this disease.
IBOGAINE: IS IT AN ACTUAL CURE FOR PARKINSONS?
Only ibogaine expresses a neurotrophin (GDNF) that resprouts dopamine
neurons, establishing a benign self-reinforcing GDNF loop. But taking
drugs right away turns the GDNF loop off. So for it to work, you have to
actually quit. GDNF also represents a neuroprotective and restorative
treatment for Parkinson’s disease. Because the disulfide-linked,
homodimeric GDNF protein cannot cross the blood-brain barrier, an
intraparenchymal catheter must be inserted to infuse the peptide directly
into the substantial nigra in the base of the brain. In a previous
clinical trial, this significantly ameliorated Parkinson’s, improving
motor skills and quality of life, which correlated with increased function
of midbrain dopaminergic neurons, as evidenced by F-dopa PET imaging.
Additional evidence suggested this enhanced cellular activity was due to
neuronal re-sprouting, an effect that is very desirable to treat drug
addiction.Unlike GDNF, ibogaine DOES cross the blood brain barrier, since the methoxy
group (which the noribogaine metabolite does not have) makes ibogaine
lipophilic. For this reason a clinical trial of ibogaine for Parkinson’s
has been pending at Columbia University for more than a year, since
ibogaine expression of GDNF is robust, and a pill you swallow is obviously
vastly superior to inserting a shunt into your head. But the DEA has
blocked the Parkinson’s trial because ibogaine is schedule I. If you don’t
want to bother Aaron Black, contact Bill Deblasio directly to get him to
circulate a letter to DEA head Michele Leonhart among the NYC
Congressional delegation. Our draft letter implores her to recommend a
different schedule for ibogaine that would encourage research. It lays out
4 reasons ibogaine has zero abuse potential and does not belong in any
schedule that has a “high potential for abuse.” This way, instead of
asking for provision of an hallucinogen for drug addicts, we’ll be
advocating a REMogenic CURE for Parkinson’s!