Ibogaine Therapy

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From a medical perspective, using buprenorphine in substitution therapy for opioid maintenance presents significant problems when a patient attempts to detox. Comparatively, ibogaine addiction interruption therapy and treatment for opioid dependence is effective for people dealing with addictions to Subutex and Suboxone. In fact, it can sometimes take 4-6 weeks or more of gradually tapering your use of buprenorphine and switching over to short-acting opioids (SAO’s), prior to receiving ibogaine therapy for op**te dependence to treat an addiction to Subutex or Suboxone.

Despite the fact that ibogaine was never approved as a medicine for the treatment of drug addiction in most western countries (Vastag, 2005; IND39,680), human experience suggested the effectiveness of single large doses of ibogaine to block withdrawal symptoms and cravings in drug dependent individuals (Sheppard, 1994; Alper et al., 1999; Mash et al., 2000, 2001; Lotsof and Alexander, 2001; Bastiaans, 2004). Self-treating he**in addicts made the original discovery in the 1960s that ibogaine eliminates the signs and symptoms of opioid withdrawal. Alper and coworkers collected data from people who took ibogaine between 1962 and 1993 with the intention of “interrupting” their he**in addiction (Alper et al., 1999). Out of 33 human subjects treated with 6–29 mg/kg ibogaine (average 19 mg/kg), 25 reported blockade of opioid withdrawal symptoms and no further desire to take he**in in the days following treatment.

According to the report published in Progress in Brain Research, a single “heaped teaspoon” of iboga root bark triggers euphoria. An ibogaine dose of 5 mg/kg of a person’s bodyweight appears to cause mostly stimulatory effects. Doses of 10 mg/kg or more of a person’s bodyweight launches a visual phase lasting 1 to 4 hours followed by an introspective stage, the latter of which gives patients insights into their addictive behaviors. Researchers have also found that ibogaine led to resolution of patients’ opioid withdrawal syndrome within 48 hours and was be effective in blocking return to use for years.

Deborah C. Mash, PhD, who has been researching ibogaine’s potential for more than 25 years and is now CEO of a company investigating the agent, told Healio Primary Care that ibogaine “targets several neurochemical systems in the brain at high doses to bring about a rapid reset that blocks opioid withdrawal and craving. Ibogaine could be developed as an in-hospital treatment similar to the medical use of brexanolone, the FDA-approved drug for postpartum depression.”

Scientists at UCSF’s Ernest Gallo Clinic and Research Center have now shown definitively in experiments with mice and rats that Ibogaine does reduce alcohol consumption, and they have determined that it does so by increasing the level of a brain protein known as glial cell line-derived neurotrophic factor, or GDNF. In a separate study, they demonstrated that GDNF by itself decreases alcohol consumption.
The research is being published in the January 19 issue of The Journal of Neuroscience.
“By identifying the brain protein that Ibogaine regulates to reduce alcohol consumption in rats, we have established a link between GDNF and reversal of addiction—knowledge of a molecular mechanism that should allow development of a new class of drugs to treat addiction without Ibogaine’s side effects,” said Dorit Ron, PhD, UCSF associate professor of neurology and also principal investigator at the Gallo Center. Ron is co-senior author of the paper with Patricia Janak, PhD, UCSF assistant professor of neurology and also principal investigator at the Gallo Center.

During the introspection phase, Ibogaine promotes psychotherapeutic effect that empowers the client to conquer fear and negative emotions that may drive their addictions. This phase allows clients to explore psychological issues and behavior patterns that support addictions and other psychological problems. Hallucinogenic and euphoric actions of psychoactive drugs normally graduate into a state of “dependency” when addiction is established. This would be the case with L*D “trips” and flashbacks. But Ibogaine’s unique psychoactivities, which are the hallucinogenic and introspective phases, are utilized as individual “therapy” that is focused, devoid of euphoria and dependency. This hallucinogenic experience or vision was characterized by “Narranjo, a psychiatrist who studied ibogaine and harmaine as oneirophrenics or dream makers from the Greek oneiros, ‘dream’ and phren ‘think’ as opposed to hallucinogens. French researchers (Goutarel, Gollnhofer and Sillans) have suggested that iboga (Ibogaine) allows people to disconnect the ‘self’ from the external reality in order to reconnect themselves to an inner reality, while still being able at any time to return to what is happening around them” (Ravalec, Mallendi, & Paicheler, 2007).

Also mysterious is how ibogaine works to disrupt the cycle of addiction. People who have tried it have likened the intense hallucinogenic trip to going through years' worth of therapy in 24 hours, with flashbacks to childhood and pivotal experiences. “It was so vivid. It was like watching a movie with your eyes closed,” says Kevin (whose name has been changed to protect his identity), who tried ibogaine for multiple addictions during a stay at a clinic in Mexico. “I had visions of me being 16 years old when I used to drink cough syrup, and my mom caught me one night and she was crying.”

Medical anthropologist Thomas Kingsley Brown, who has worked with the Multidisciplinary Association for Psychedelic Studies in California, conducted an unpublished study that followed 30 chronic drug users for a year after receiving ibogaine therapy at two clinics in Mexico. Brown says he and his colleagues called patients every month and gave them a questionnaire called the Addiction Severity Index, which measures progress in several problem areas commonly related to addiction, such as psychiatric and social well-being. Two thirds of the patients made it halfway through the study before dropping out; one third completed all 12 months. The preliminary data showed that all patients benefited from what Brown calls a “huge reduction in withdrawal symptoms.” Those who completed the year had significant improvements in social well-being. The study did not follow them further, so Brown does not know how many, if any, relapsed into drug use.

The indole alkaloid ibogaine (NIH 10567, Endabuse) is currently being examined for its potential utility in the treatment of co***ne and opioid addiction.Radioligand binding assays targeting over 50 distinct neurotransmitter receptors, ion channels, and select second messenger systems were employed to establish a broad in vitro pharmacological profile for ibogaine. These studies revealed that ibogaine interacted with a wide variety of receptors at concentrations of 1-100 microM. These included the mu, delta, kappa, op**te, 5HT2, 5HT3, and muscarinic1 and 2 receptors, and the dopamine, norepinephrine, and serotonin uptake sites. In addition, ibogaine interacted with N-methyl-D-aspartic acid (NMDA) associated ion and sodium ion channels as determined by the inhibition of [3H]MK-801 and [3H]bactrachotoxin A 20-alpha-benzoate binding (BTX-B), respectively. This broad spectrum of activity may in part be responsible for ibogaine's putative anti-addictive activity.

Ibogaine act on several neurotransmitter systems in the brain, potentially contributing to an ability to suppress autonomic changes, objective signs, and subjective distress associated with op**te withdrawal. They interact with acetylcholine, serotonin, and dopamine systems, as well as show a micromolar affinity to numerous receptor sites such sigma receptors, kappa- and mu-opioid receptors, and the N-methyl-D-aspartate ion channel.

Ibogaine proponents say it does a better job because it works on many neural pathways at the same time, not just one, as do other treatments. Buoyed by these ideas, two companies, one with partial funding from the National Institute on Drug Abuse (a federal research agency), are currently developing medications based on ibogaine derivatives.

Around that time the late Howard Lotsof, then a 19-year-old he**in addict, took some ibogaine for its hallucinogenic effects and told other addicts the drug also reduced his he**in cravings. Word spread, and addicts began using larger doses, up to 20 milligrams per kilogram (mg/kg) of body weight, to help kick their habits. Some animal studies of ibogaine and addiction came out in the late 1980s, and they suggested the substance did curb withdrawal symptoms. The overseas clinics began to open.

But experiences with ibogaine vary from person to person—not everyone, for instance, experiences the drug's trippy effects—and its neurochemistry and biophysics are perplexing. Research indicates that ibogaine acts on dopamine, serotonin and other neurotransmitter pathways strongly linked to addiction and reward, similar to other psychedelics currently being explored for addiction and mental illness treatment. Yet preliminary studies suggest that ibogaine attaches to other molecules in a unique way. “The mechanism of action at the molecular level is peculiar,” wholly unlike that of “traditional” drugs, says Emeline Maillet, a co-author of the 2015 study on rats and ni****ne, who was then at DemeRx in Miami. Most active compounds work by binding to a receptor on the outside of a cell membrane. But ibogaine seems to do the opposite, binding to the inside of the membrane—something no other naturally occurring molecule is known to do, says Maillet, who observed this effect in another 2015 study examining ibogaine's effect on opioid receptors.
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For decades research on ibogaine has been stymied by its classification as a Schedule I drug, the most tightly regulated category. Yet the results of animal studies have been intriguing. In May 2016 a meta-analysis examining 32 such studies, mostly in mice and rats, found that ibogaine reduced self-administration of co***ne, opioids and alcohol. An earlier study from 2015 found that noribogaine, the substance that ibogaine breaks down to when ingested, reduced self-administration of ni****ne in addicted rats by 64 percent.

Ibogaine is a tryptamine. Its action is complex, affecting several different neurotransmitters at the same time. It appears to possess important affinities for N-methyl-d-aspartate (NMDA), kappa-opioid, sigma, and ni****ne receptors. Ibogaine's action at the kappa-opioid receptor is likely to contribute to its psychoactive effects (Zubaran et al., 1999). It is thought that the weak agonistic action of ibogaine on the serotonin 5HT2A receptor (Glick and Maisonneuve, 1998; Helsley et al., 1998) may contribute to its hallucinogenic effects (Wei et al., 1998). Dopamine levels are not only lowered by ibogaine, but also its breakdown is enhanced (Glick et al., 2001). Ibogaine may work in reversing the effects of op**tes on gene expression, with resulting impacts on neuroreceptors, returning them to a pre-addiction condition (Brackenridge, 2010). Furthermore, addictive loops and pathways in the brain are reversed (He et al., 2005).

From preclinical studies conducted in Holland on 30 American he**in addicts (volunteers) by NIDA,it was reported that two-thirds of the group remained drug free for the periods from 4 months to 4 years from a single administration of IBOGAINE HCL, the synthetic form of IBOGAINE.Furthermore,the report underlined that when IBOGAINE is administered to people seeking to beat addiction to he**in,alcohol,co***ne or tobacco,the product achieves two major things:

Firstly,there is complete removal or severe attenuation of the symptoms of withdrawal,allowing the addict to detox painlessly.

Secondly,there is the removal of the desire to use drugs for a more or less long period.Follow-up dosing maybe undertaken at three monthly intervals should the patient wish it.

Ibogaine is the major constituent of the root of Tabernanthe iboga, a shrub commonly found in West and Central Africa. Ibogaine has been shown to reduce co***ne and morphine self-administration in laboratory animals and to attenuate alcohol intake by alcohol-preferring rats. The compound also reduces the rewarding effects of ni****ne in animals. In addition, the compound reduces craving in humans. Ibogaine is thus a potentially useful anti-addictive agent.

In the other study, researchers in New Zealand concluded that a single treatment with ibogaine reduced symptoms of opioid withdrawal in people dependent on opioids over 12 months. It also helped people stop taking opioids or maintain a reduced use.

In France, ibogaine was sold and prescribed as an antidepressant and stimulant called Lambarene for more than 30 years until the 1960s, when the government outlawed the sale of ibogaine. But its antiaddictive effects weren’t well known in the U.S. until 1962, when Howard Lotsof—then a 19-year-old completely outside the medical establishment—experimented with it and noticed it wiped out his he**in addiction. It did the same for several of Lotsof’s peers when he organized 20 lay drug experimenters, all in their late teens and early 20s, to try many hallucinogens including ibogaine.

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In 1991, the National Institute on Drug Abuse (NIDA) decided to fund animal research into ibogaine; the resulting studies (and later ones) in rodents found that ibogaine reduced how much he**in, morphine, co***ne and alcohol the animals consumed. This work primed the U.S. Food and Drug Administration (FDA) to greenlight a clinical trial of ibogaine in humans for co***ne dependence, but it fell apart in early stages because of a lack of funding and contractual disputes.

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Ibogaine also elevates serotonin concentrations in the brain, a possible explanation for its antidepressive effects. The sustained presence of ibogaine in the CNS coupled with its agonist activity at opioid receptors may produce the self-tapering effect in op**te-dependent patients following abrupt discontinuation of op**tes.

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**teskill

Ibogaine and Noribogaine act on several neurotransmitter systems in the brain, potentially contributing to an ability to suppress autonomic changes, objective signs, and subjective distress associated with op**te withdrawal. They interact with acetylcholine, serotonin, and dopamine systems, as well as show a micromolar affinity to numerous receptor sites such sigma receptors, kappa- and mu-opioid receptors, and the N-methyl-D-aspartate ion channel.
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**teaddiction

Ibogaine is a dissociative psychedelic with oneiric properties that has multiple aforementioned anti-addictive mechanisms, as well as the ability to generate therapeutic psychological insights, suggesting promise in treating alcohol use disorders.

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Ibogaine is the major constituent of the root of Tabernanthe iboga, a shrub commonly found in West and Central Africa. Ibogaine has been shown to reduce co***ne and morphine self-administration in laboratory animals and to attenuate alcohol intake by alcohol-preferring rats. The compound also reduces the rewarding effects of ni****ne in animals. In addition, the compound reduces craving in humans. Ibogaine is thus a potentially useful anti-addictive agent.

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Ibogaine has unique and complex pharmacological properties, including a broad spectrum of binding on receptors sites as an agonist (hallucinogenic) and antagonist (antiaddictives). This reflects its peculiar clinical characteristics. The primary target sites are the NMDA, nicotinic, σ-, κ-opioid, and μ-receptors. NMDA are receptors of the messengers of glutamate, calcium, aspartate, amino acid, and glycine.

Ibogaine demonstrates complex, broad, and novel pharmacological mechanisms of action to consider in the potential treatment of alcohol use disorders. The alkaloid has low micromolar affinity for μ and κ opioid receptors, σ1 and σ2 receptors, serotonin reuptake transporter (SERT) and dopamine transporter (DAT), and is an N-methyl-d-aspartate (NMDA) and α3β4 nicotinic acetylcholine receptor (nAChR) antagonist that increases glial-derived neurotrophic factor (GDNF) expression and substance P immunoreactivity.

Ibogaine is a dissociative psychedelic with oneiric properties that has multiple aforementioned anti-addictive mechanisms, as well as the ability to generate therapeutic psychological insights, suggesting promise in treating alcohol use disorders.