"Narcotic Addiction Syndrome" A' quick prognosis! Ibogaine in the treatment of Heroin withdrawal.
Ibogaine is a naturally occurring psychoactive indole alkaloid derived from the roots of the rain forest shrub Tabernanthe Iboga.
It has been seen that the alkaloid reduces craving for opiates and other illicit drugs, and has ameliorative effects in acute opiate withdrawal .
Ibogaine works for certain problems like substance abuse and certain psychological disorders.
Now, soldiering on, I will try to, at least to some extent, explain the exact chemical mechanisms that are involved so that Ibogaine can do its job so efficiently, without causing death by boredom to the reader. This could also to some extent explain why Ibogaine is not for everybody, and why anyone considering taking Ibogaine should do proper research on the subject and contact a reliable, knowledgeable and trained provider to ensure his or her safety during the experience.
To start off with, let us look at some of the mechanisms in the brain that influences consciousness, behaviour, and mood. I shall only go into some detail for two of the mechanisms that are influenced by Ibogaine. And also, because this is Ibogaine SA’s interest, concentrate on the mechanisms involved in substance abuse.
The fact is, Ibogaine reaches a high concentration in the brain of rats after intra-peritoneal (Skin of the stomach)injection, and its effects may be the result of complex interactions between multiple neurotransmitter systems. This is what scares scientists from researching Ibogaine – the difficulties predicting and explaining exactly what happens when more than one body or neurological system undergoes changes. Now- an addictive drug can be called such when it activates, in some way, the brain reward systems, which produces feelings of euphoria, a perception of undue increased wellness, or a perceived enhancement of social abilities. One of the most important neurotransmitters in the brain that are involved in this mechanism is Dopamine – the brain’s own feel-good drug. It appears that dopamine, because of it’s role in motivation reward processes, is instrumental in causing some forms of clinical depression (due dopamine’s unusually low levels in the synaptic cleft where it produces its effects by binding with dopamine receptors). Dopamine, in order to have an effect, is stored in a cellular structure. It is then released into a synaptic cleft (Space) before it is recognised on the other side by another structure (Receptor), which then causes the "feel good" effect of dopamine. The dopamine is then released from the post-synaptic structure and re-absorbed by the store. This balance is a carefully controlled mechanism that regulates the continuous release, binding and re-uptake of dopamine. Heroin and other "downers" increases the neuronal firing rate of dopamine cells (Causing quicker than normal release of dopamine from the "stores"), while Cocaine and other "uppers" inhibits the re-uptake of dopamine (thereby blocking the moving back of dopamine into storage). The effect of either is an over supply of dopamine at the post-synaptic receptor, and a resulting good feeling. When the two substances are combined, they produce even more intense dopamine activation (More free dopamine in the synaptic cleft = more binding to receptors = euphoria).
In addition to their acute effects described above, repeated use of psychomotor stimulants like cocaine and opiates (like heroin) causes changes in the mesolimbic dopamine system. This effect, over a longer term, can negatively influence the ability of the dopamine receptors to recognise dopamine, so that a constant oversupply of dopamine is needed in the synaptic cleft to feel "normal". This could explain why it is so easy to relapse after long-term use of crystal methamphetamine, or tik, which seemingly causes more severe damage to the mesolimbic dopamine system than most other drugs: If a person ceases to use tik, there is almost certainly an acute shortage of dopamine in the synaptic cleft, and it inevitably leads to a severe, long-term depression. The only way to reverse this effect, is by rebuilding of the dopamine receptors.
This reconstruction of the receptors is helped on by a factor called GDNF (Glial cell line-derived Neurotrophic Factor), which without help, is a long and time-consuming (Up to six months in some instances) process. This is where Ibogaine comes into the picture: It acts as a catalyst for GDNF. I.e. it causes more rapid reconstruction of the structures inside the brain that was damaged through long-term use of addictive drugs. It makes the after-effects of drugging disappear quicker than without Ibogaine intervention. A second brain chemical, Serotonin, also plays an important role in the human brain. Some refer to it as a "molecule of happiness". Serotonin is produced in the Pineal Gland which lies deep in the centre of the human brain. Serotonin plays an instrumental part in the regulation of numerous functions in the body like the control of appetite, sleep, memory and learning, mood, behaviour, and depression, and cardiovascular function. (Do you recognise the similarity of these disturbances when compared with behavioural changes often seen with drug addicts?) Serotonin production can be influenced by lifestyle, for instance, and regular exercise and Omega 3 can increase production. If one looks at the chemical structure of Ibogaine, there is a remarkable similarity to the chemical structure of Serotonin. In a similar fashion as with dopamine, serotonin can have an effect on the level of consciousness, and because Ibogaine binds to the sites that are supposed to recognise serotonin, there is once again an acute, but short-lived over-supply of serotonin (Ibogaine blocks the Serotonin from binding to it’s work-place), thereby re-directing it to the "older" parts of the brain, where the blood stream takes it to the sense interpretive centres and the parts that control movement. (LSD, another hallucinogenic compound, has a similar effect). This may explain why the user of Ibogaine experiences a state of "awake dreaming" and severe loss of co-ordination while under the influence of Ibogaine. This is the acute effect on this system.
After the initial flood, which lasts for the first hours after taking Ibogaine, the Ibogaine passes through the liver, and is turned into Noribogaine, which is also active in a similar way to Ibogaine. In addition, the Ibogaine is a fat-soluble
compound, which causes that it to stay inside the body for an extended period of time. It is released into the blood-stream over a period of time, and converted to Noribogaine. So, although the half life (An indication of how long a drug is active) of Ibogaine and Noribogaine is short, the effects, especially on the serotonergic systems, last for an extended period of time. The Noribogaine, in it’s turn, then acts as a serotonin uptake inhibitor, thereby preventing depression, because more free serotonin is available in the synoptic cleft, but not enough to be "washed" to the pre-mentioned older parts of the brain to cause ongoing hallucinations and lack of co-ordination. The most concrete evidence for the connection between serotonin and depression is the decreased concentrations of serotonin metabolites in the cerebrospinal fluid and brain tissues of depressed people. This may also explain the Euphoric feeling that a person who took Ibogaine may experience for a period of time.
Another important mechanism of action of Ibogaine, is that it acts as a non-competitive NMDA antagonist on the Glutamate receptors, which plays a role in the learning process of addiction, it acts as Mu and Kappa receptor agonists (Second Level), i.e. it potentiates the effects of opiates (And at the same time reduces the need for them), which explains the danger involved when using Heroin and Ibogaine together.
+++
(Brian Vastag - The Journal of the American Medical Association Vol. 288 No. 24, pp. 3096-3101, December 25, 2002)
