139 replies to this topic

[mycotheologist]

Ooh.. phenibut.. horrible stuff for WD'ing from. If it's worth a dollar to anyone, I found that the medication OXCARBAZEPINE was really good for benzo withdrawals. I found theanine actually made everything worse, interestingly enough...

True but I find that benzos completely counteract all phenibut w/d symptoms. I don't think there is any significant cross tolerance between phenibut and benzos because when I take a benzo after a phenibut binge, I only need a very low dosage and vice versa. However, I tried circumventing addiction by using phenibut for a week, then switching to a benzo for a week and when I quit, there was no acute withdrawal but there was this residual nervousness, anxious feeling. I'm quitting everything now since its the summer (and I'm off college) so I'll see how long it takes for this residual w/d symptom to disappear. Either way, the acute phenibut withdrawal can be circumvented using a benzo and I've heard others claim that the acute benzo withdrawal can be circumvented with phenibut. Thats obviously much trickier since you can't use phenibut for more than a week without getting addicted to it.

Edited by mycotheologist, 09 July 2012 - 06:10 PM.

[ScienceGuy]

ScienceGuy: You provide lots of good info but you are you sure GABA_a and GABA_b receptor agonists exhibit significant cross tolerance? For example, could baclofen not be used to help with benzo w/d symptoms without prolonging the withdrawal?

It is common for substances that possess and affinity for the GABA-A RECEPTOR to have at least some affinity for the GABA-B RECEPTOR albeit in some instancs to a much lesser extent, and vice versa; hence, without since it is often difficult to be absolutely sure what is the particular status in this regard for a particular GABA AGONIST my advice is to steer clear of all GABA RECEPTOR AGONISTS completely... better safe than sorry

Futhermore, there are much better options with regards to substances that can be taken to assist matters which are not GABA RECEPTOR AGONISTS.

Also, you say its best to use a short acting benzo to taper down. Its the other way around. You should use a long acting one like diazepam or clonazepam because longer acting benzos self taper and thus, give much milder withdrawals.

Sorry, I should have made this point more clearly. You are absolutely correct that the standard medical recommendation when commencing withdrawing from HIGH-POTENCY SHORT-ACTING BENZOS is to switch to a LONG-ACTING BENZO for the initial part of the tapering down process, with the intention of reducing the liklihood of rebound withdrawal symptoms occurring between doses. However, if one is in fact already quite a way down the road with regards to the tapering down process or if one is withhdrawing from taking either a MEDIUM or LONG ACTING BENZO then this phenomen is very unlike to occur; and in these cases it can in fact be most helpful to switch to a SHORT-ACTING BENZODIAZEPINE (preferably LOW-POTENCY) such that your GABA RECEPTORS are not hit 24/7 and hence can begin to recover. This is especially applicable if you wish to concommitently use BACOPA MONNIERI to help upregulate your GABA system.

You say to avoid all GABAergics during benzo withdrawals but I'm sure there is a difference between using an addictive GABAergic such as gabapentin to using a non addictive one such as kola gotu to manage PAWs. At the very worst, you will be temporarily fending off the w/d symptoms using the non addictive substance, you won't end up further downregulating your GABA receptors. With that in mind, they are good tools to have to give you some temporary relief from the withdrawal symptoms when you need it. Thats pure speculation on my part I have no practical experience with this.

Ah, this is a common misunderstanding... Please kindly note that despite their names neither GABAPENTIN nor PREGABALIN has an affinity for the GABA RECETPORS, hence neither's mechanism of action is that of GABA RECEPTOR AGONIST.

It is totally understandble how you would mistakenly assume that these two drugs are GABAergics given their names both include the word GABA; however, this is purely unhelpful and confusing name selection. However, there is an entirely different reason why I strongly advise against prolonged usage of either GABAPENTIN or PREGABALIN, which has nothing to do with the GABA system, which is that both drugs strongly inhibit proper IMMUNE FUNCTION, including suppressing white blood cell count. Therefore, you are likely to fix one problem only to cause another, more serious problem.

What about you ScienceGuy, do you have much experience with GABAergic withdrawals...

YES. I have within clinical practice treated many types of ADDICTION and subsequent WITHDRAWAL

...or are you speaking purely from theoretical knowledge?

NO

Also, I read that kavalactones aren't actually GABA agonists but rather they work by upregulating GABA_a receptors.

KAVA KAVA (PIPER METHYSTICUM):

CNS Drugs 2002;16(11):731-43.

Therapeutic potential of kava in the treatment of anxiety disorders.

Singh YN, Singh NN.

Source
College of Pharmacy, South Dakota State University, Brookings, South Dakota 57007, USA. yadhu_singh@sdstate.edu

Abstract
Anxiety disorders are among the most common psychiatric disorders that affect all age groups of the general population. Currently, the preferred treatment is with pharmacological drugs that have antidepressant or anti-anxiety properties. However, these agents have numerous and often serious adverse effects, including sedation, impaired cognition, ataxia, aggression, sexual dysfunction, tolerance and dependence. Withdrawal reactions on termination after long-term administration are also a major limiting factor in the use of these agents. Herbal remedies, including kava (Piper methysticum), have been shown to be effective as alternative treatments, at least in mild to moderate cases of anxiety. Kava is a social and ceremonial herb from the South Pacific. It is available in the west as an over-the-counter preparation. Its biological effects, due to a mixture of compounds called kavalactones, are reported to include sedative, anxiolytic, antistress, analgesic, local anaesthetic, anticonvulsant and neuroprotective properties. The pharmacological properties of kava are postulated to include blockade of voltage-gated sodium ion channels, enhanced ligand binding to gamma-aminobutyric acid (GABA) type A receptors, diminished excitatory neurotransmitter release due to calcium ion channel blockade, reduced neuronal reuptake of noradrenaline (norepinephrine), reversible inhibition of monoamine oxidase B and suppression of the synthesis of the eicosanoid thromboxane A(2), which antagonises GABA(A) receptor function. Clinical studies have shown that kava and kavalactones are effective in the treatment of anxiety at subclinical and clinical levels, anxiety associated with menopause and anxiety due to various medical conditions. Until recently, the adverse effects attributed to kava use were considered mild or negligible, except for the occurrence of a skin lesion. This disorder, called kava dermopathy, occurs only with prolonged use of large amounts of kava and is reversible on reduced intake or cessation. Rare cases of interactions have occurred with pharmaceutical drugs that share one or more mechanisms of action with the kavalactones. In the past few years, about 35 cases of severe liver toxicity associated with kava intake have been reported in Europe and the US. However, a direct causal relationship with kava use has been difficult to establish in the majority of the cases, and there is insufficient evidence to implicate kava as the responsible agent. Nevertheless, until further research clarifies any causality, kava should be used with caution.
PMID: 12383029

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Planta Med. 2001 Jun;67(4):306-11.

Interaction of various Piper methysticum cultivars with CNS receptors in vitro.

Dinh LD, Simmen U, Bueter KB, Bueter B, Lundstrom K, Schaffner W.

Source
Institute of Pharmaceutical Biology, University of Basel, Witterswil, Switzerland.

Abstract
Methanolic leaf and root extracts of the Hawaiian kava (Piper methysticum Forst.) cultivars, Mahakea, Nene, Purple Moi and PNG, were tested on binding affinities to CNS receptors including GABAA (GABA and benzodiazepine binding site), dopamine D2, opioid (mu and delta), serotonin (5-HT6 and 5-HT7) and histamine (H1 and H2). HPLC analysis was carried out in order to determine the amount of the main kavalactones kavain, 7,8-dihydrokavain, methysticin, 7,8-dihydromethysticin, yangonin and 5,6-demethoxyyangonin. The most potent binding inhibition was observed for leaf extracts to GABAA receptors (GABA binding site) with IC50 values of approximately 3 micrograms/ml, whereas root extracts were less active with IC50 values ranging from 5 micrograms/ml (Nene) to 87 micrograms/ml (Mahakea). Since the leaf extracts generally contained lower amounts of the kavalactones than the root extracts, there might exist additional substances responsible for these activities. Leaf extracts also inhibited binding to dopamine D2, opioid (mu and delta) and histamine (H1 and H2) receptors more potently than the corresponding root extracts with IC50 values ranging from 1 to 100 micrograms/ml vs. > or = 100 micrograms/l, respectively. Significant differences in the potential of binding inhibition were also observed between cultivars. Binding to serotonin (5-HT6 and 5-HT7) and benzodiazepine receptors was only weakly inhibited by both root and leaf extracts of all four cultivars. In conclusion, our investigation indicates that the GABAA, dopamine D2, opioid (mu and delta) and histamine (H1 and H2) receptors might be involved in the pharmacological action of kava extracts. Since the cultivars contained similar amounts of kavalactones, while their pharmacological activities differed markedly, other constituents may play a role in the observed activities. Additionally, leaves generally exhibited more potent binding inhibition than roots, therefore leaf of P. methysticum might be an interesting subject for further pharmacological studies.

Brilliant info though, I learned a lot from reading your posts.

Thank you. It is always lovely to receive positive feedback.

Do you have any more info on the things that do work?

Have you read THIS thread?: TREATING ANXIETY SAFELY & EFFECTIVELY

For the past 6 months, I have been switching between phenibut and GABA_a agonists...

PHENIBUT is an AGONIST of both GABA-B and GABA-A RECEPTORS so, even though its affinity is stronger for the GABA-B RECEPTOR its agonism of the GABA-A receptor is significant and hence I am afraid to say you haven't been 'switching' at all... in that you have been 'switching' from GABA-A AGONISTS to GABA-A & GABA-B AGONIST

PHENIBUT in my opinion is horrible stuff and should be avoided at all costs; it is ADDICTIVE and its WITHDRAWAL is unpleasant.

...and I'm worried about how long it will take me to recover. I quit for 3 weeks after taking valium and I was actually able to sleep every night but I had this nervous/anxious feeling for a good while. I ended up getting back into this vicious cycle again though so I've been on phenibut now for 10 days.

Your problem is that you have not been properly carrying out a tapering down of GABA RECEPTOR AGONISTS.

My advice is to ditch the PHENIBUT completely and begin a proper tapering down program using DIAZPEPAM (VALIUM) as the only GABA RECEPTOR AGONIST, and add to this BACOPA MONNIERI concurrently. At some point it will be advantagious to switch from DIAZPEPAM (VALIUM) to a LOW-POTENCY SHORT-ACTING BENZO to begin to give your receptors a break and allow the BACOPA to work its magic more effectively.

Edited by ScienceGuy, 09 July 2012 - 07:36 PM.

[ScienceGuy]

Ooh.. phenibut.. horrible stuff for WD'ing from. If it's worth a dollar to anyone, I found that the medication OXCARBAZEPINE was really good for benzo withdrawals. I found theanine actually made everything worse, interestingly enough...

True but I find that benzos completely counteract all phenibut w/d symptoms. I don't think there is any significant cross tolerance between phenibut and benzos because when I take a benzo after a phenibut binge, I only need a very low dosage and vice versa. However, I tried circumventing addiction by using phenibut for a week, then switching to a benzo for a week and when I quit, there was no acute withdrawal but there was this residual nervousness, anxious feeling. I'm quitting everything now since its the summer (and I'm off college) so I'll see how long it takes for this residual w/d symptom to disappear. Either way, the acute phenibut withdrawal can be circumvented using a benzo and I've heard others claim that the acute benzo withdrawal can be circumvented with phenibut. Thats obviously much trickier since you can't use phenibut for more than a week without getting addicted to it.

Oh lordy... no no no!

You are taking GABA RECEPTOR AGONISTS to treat the withdrawal symptoms of GABA RECEPTOR AGONIST... that's like drinking A DOUBLE VODKA to treat ALCOHOL WITHDRAWAL

See my advice in my previous post regarding what you should do.

Edited by ScienceGuy, 09 July 2012 - 07:42 PM.

[gamesguru]

Going cold turkey is not advised, as this has been frequently noted to increase susceptibility to protracted withdrawal symptom (post-acute withdrawal lasting 6 months to 3 years). I'd like to assure you that everything will return to normal, but there is evidence that there are long-term affects on cognition (http://www.ncbi.nlm....pubmed/15033227) and physical health (http://www.benzo.org.uk/pws04.htm). I can assure you that things will only improve. If you've been off of them for over a year now, I'm not sure I can agree with ScienceGuy's recommendation to begin Valium, as you're already deep into the protracted withdrawal.

Valerian is an allosteric modulator of GABA-A receptors, so it would, theoretically, be useful in treating withdrawals. You need to try a higher dose if you didn't respond. Though, again, being so deep into protracted withdrawal, there's no real point in trying to taper off. In my opinion, you should just ride it out. If anything, you should look for things to improve cognition and upregulate GABA receptors (as Bacopa may do, though not certainly). Piracetam, choline, and others may be worth trying to alleviate foggy thinking. Maybe it's just time to accept the damage that has been done and just ride out the healing process?

[ScienceGuy]

Ooh.. phenibut.. horrible stuff for WD'ing from.

I could not agree more... HORRIBLE stuff!

If it's worth a dollar to anyone, I found that the medication OXCARBAZEPINE was really good for benzo withdrawals.

Excellent suggestion, although being ANTI-CHOLINERGIC it should be noted that it IMPAIRS COGNITIVE FUNCTION (so you probably don't want to time taking it with having to carry out any especially mentally demanding tasks such as examinations etc...) and it does have the potential to cause an array of other side effects. Even so, it is most certainly a potentially useful tool in treating BENZO WITHDRAWAL none-the-less... so nice one suggesting it!

I found theanine actually made everything worse...

Unfortunately this is not uncommon

[ScienceGuy]

I'm not sure I can agree with ScienceGuy's recommendation to begin Valium, as you're already deep into the protracted withdrawal.

Hey dasheenster,

You misunderstand. My advice is not directed at QUAMQUAM91, but in reply to MYCOTHEOLOGIST, who has stated "For the past 6 months, I have been switching between phenibut and GABA_a agonists and I'm worried about how long it will take me to recover" and has been taking VALIUM.

My advice to QUAMQUAM91 is to steer well clear of any and all GABA RECEPTOR AGONISTS and to start taking BACOPA immediately.

Edited by ScienceGuy, 09 July 2012 - 08:01 PM.

[mycotheologist]

It is common for substances that possess and affinity for the GABA-A RECEPTOR to have at least some affinity for the GABA-B RECEPTOR albeit in some instancs to a much lesser extent, and vice versa; hence, without since it is often difficult to be absolutely sure what is the particular status in this regard for a particular GABA AGONIST my advice is to steer clear of all GABA RECEPTOR AGONISTS completely... better safe than sorry

True, alcohol, if I'm not mistaken, binds primarily to GABA_a receptors but it clearly has some affinity to GABA_b receptors too since it exhibits cross tolerance with GHB. However, baclofen is the GABAergic of choice for managing alcohol withdrawal symptoms since it exhibits relatively low cross tolerance.

Futhermore, there are much better options with regards to substances that can be taken to assist matters which are not GABA RECEPTOR AGONISTS.

I read all your posts in this thread, the one you mentioned which I'm going to try out on this phenibut w/d is l-theanine. I like the fact that it has some glutamate antagonist properties because it should help protect against brain damage (caused by glutamate excitotoxicity). So far, the only non GABAergics I have tried during GABAergic withdrawals are amphetamines and opioids. Amphetamines was a huge mistake (not surprising lol). Opioids seem to make things worse too.

Ah, this is a common misunderstanding... Please kindly note that despite their names neither GABAPENTIN nor PREGABALIN has an affinity for the GABA RECETPORS, hence neither's mechanism of action is that of GABA RECEPTOR AGONIST.

Thanks for clearing that up. I'm a chemistry student so I have the habit of trying to predict the SARs myself by looking at the structures. Doesn't always work out too well lol. Both of those molecules are GABA analogues so I assumed they mimic the neurotransmitter.

YES. I have within clinical practice treated many types of ADDICTION and subsequent WITHDRAWAL

The world needs more people like you. Withdrawals from downers can be pretty horrific, the more knowledge we attain, the better we'll be able to deal with them. When I get my masters in a chemistry/pharmacology related field, I want to research ibogaine analogues because I suspect that molecule may propel us into a new paradigm in which drug addiction isn't the seemingly inescapable nightmare that it is for many people (i.e. people who can't just drop everything and dedicate a few weeks to recovering).

Ah shit, you're right. Now I'm worried. Hopefully phenibut has very low GABA(A) activity. I have some xanax coming in a few days but all I have right now is phenibut. I can get some diazepam from a doctor if I really need to. My plan is to just use the xanax to sleep for a week, then taper down off it.

Edited by mycotheologist, 09 July 2012 - 09:10 PM.

[ScienceGuy]

True, alcohol, if I'm not mistaken, binds primarily to GABA_a receptors but it clearly has some affinity to GABA_b receptors too since it exhibits cross tolerance with GHB. However, baclofen is the GABAergic of choice for managing alcohol withdrawal symptoms since it exhibits relatively low cross tolerance.

The fact that BACLOFEN is the GABAergic of choice for managing ALCOHOL WITHDRAWAL symptoms does not mean it is the best choice of substance for managing alcohol withdrawal symptoms.

METHADONE is a drug of choice for treating HEROINE WITHDRAWAL but that's not the best choice either; and personally I strongly recommend against its usage as one is simply replacing one addiction with another.

I read all your posts in this thread, the one you mentioned which I'm going to try out on this phenibut w/d is l-theanine. I like the fact that it has some glutamate antagonist properties because it should help protect against brain damage (caused by glutamate excitotoxicity). So far, the only non GABAergics I have tried during GABAergic withdrawals are amphetamines and opioids. Amphetamines was a huge mistake (not surprising lol). Opioids seem to make things worse too.

See how you get on with THEANINE. In my experience it is highly unpredictable with regards to how each person responds to it. For some individuals it can be a magic bullet and find it is wonderful; but others react badly to it, in which case it would make your withdrawal symptoms worse. You will need to ascertain whether you are a positive or negative responder to it.

Further to this I recommend that you consider self-adminstering the following cocktail of substances:

1) MAGNESIUM - For someone in your situtation I'd recommend a combination of MAGNESIUM L-THREONATE taken PER ORALLY during the day (it may assist your studies too ) plus MAGNESIUM SULPHATE administered TRANSDERMALLY via adding 1-2 cups to a HOT BATH into which you soak for at least 12 MINUTES DAILY. MAGNESIUM is not a magic bullet, but it is a very effective and useful tool in treatiing BENZO WITHDRAWAL. Incidentally, please kindly note that MAGNESIUM's primary mechanism of action as ANXIOLYTIC is NMDA RECEPTOR ANTAGONIST so provides the protection against GLUTAMATE NEUROTOXICITY that you seek.

2) BACOPA MONNIERI EXTRACT - to commence UPREGULATION and hence RECOVERY of your GABA SYSTEM. It exerts an ANXIOLYTIC effect so will help with the withdrawal symptoms. READ THIS:

Epilepsy Behav. 2010 Apr;17(4):441-7. Epub 2010 Feb 11.

Behavioral deficit and decreased GABA receptor functional regulation in the cerebellum of epileptic rats: effect of Bacopa monnieri and bacoside A.

Mathew J, Peeyush Kumar T, Khan RS, Paulose CS.

Source
Department of Biotechnology, Molecular Neurobiology and Cell Biology Unit, Centre for Neuroscience, Cochin University of Science and Technology, Kerala, India.

Abstract
In the present study, the effects of Bacopa monnieri and its active component, bacoside A, on motor deficit and alterations of GABA receptor functional regulation in the cerebellum of epileptic rats were investigated. Scatchard analysis of [(3)H]GABA and [(3)H]bicuculline in the cerebellum of epileptic rats revealed a significant decrease in B(max) compared with control. Real-time polymerase chain reaction amplification of GABA(A) receptor subunits-GABA(Aalpha1), GABA(Aalpha5,) and GABA(Adelta)-was downregulated (P<0.001) in the cerebellum of epileptic rats compared with control rats. Epileptic rats exhibit deficits in radial arm and Y-maze performance. Treatment with B. monnieri and bacoside A reversed these changes to near-control levels. Our results suggest that changes in GABAergic activity, motor learning, and memory deficit are induced by the occurrence of repetitive seizures. Treatment with B. monnieri and bacoside A prevents the occurrence of seizures thereby reducing the impairment of GABAergic activity, motor learning, and memory deficit.
PMID: 20153260

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And specifically to reverse the effects of Diazepam on the benzodiazepine pathway:

Psychopharmacology (Berl) 2008 Sep;200(1):27-37. Epub 2008 Jan 13.

Bacopa monniera exerts antiamnesic effect on diazepam-induced anterograde amnesia in mice.

Prabhakar S, Saraf MK, Pandhi P, Anand A.

Source
Department of Neurology, Post Graduate Institute of Medical Education and Research, Sector-12, Chandigarh, 160012, India.

Abstract

RATIONALE:

As Benzodiazepines are known to produce amnesia by involvement of the GABAergic system, we examined Bacopa monniera, an herb known for memory enhancement for reversal of memory deficits caused by diazepam.

OBJECTIVES:

The objective of the study was to study the effect of standardized extract of B. monniera on diazepam-induced amnesia in mice using Morris water maze.

MATERIALS AND METHODS:

We used the rota rod test as a screening measure for muscle incoordination followed by the Morris water maze scale to evaluate the effect of B. monniera on amnesia. The index of acquisition and retrieval was recorded with varying doses of Bacopa.

RESULTS:

The results revealed antiamnesic effects of B. monniera (120 mg kg(-1) oral) on diazepam (1.75 mg kg(-1) intraperitoneal)-induced amnesia. The degree of reversal by Bacopa was significant as it progressively reduced escape latency time when mice treated with diazepam were subjected to acquisition trials.

CONCLUSIONS:

The antiamnesic effects of Bacopa suggest likely a gamma-aminobutyric acid-benzodiazepine pathway possibly affecting long-term potentiation.

PMID: 18193203

3) AFOBAZOLE - This is an effective ANXIOLYTIC that also UPREGULATES the GABA SYSTEM and hence should be especially useful in treating BENZO withdrawal. READ THIS:

Bulletin of Experimental Biology and Medicine, Vol. 151, No. 5, September, 2011 PHARMACOLOGY AND TOXICOLOGY

Effects of Afobazole on the Content of Neurotransmitter Amino Acids in the Striatum in Global Transient Ischemia

V. S. Baykova, I. A. Kadnikov, M. V. Voronin, T. S. Ganshina, A. V. Gnezdilova, A. A. Gorbunov, P. C. Mirzoyan, and S. B. Seredenin

EDITED FROM FULL TEXT:

The objective of this study was to investigate delayed effects of afobazole on the levels of neurotransmitter amino acids in brain structures…

GABA level was significantly decreased in the striatum of ischemic rats. After afobazole administration, GABA level improved and reached the control values recorded in intact animals…

Afobazole administration resulted in restitution of striatal GABA content, which approached the control values; this should promote recovery of neuroprotective systems related to inhibitory influences…

Afobazole administration to ischemic animals resulted in more substantial increase in taurine level in the striatum. Agonistic interaction between afobazole and σ1-receptors, possibly underlies this phenomenon…

Thus, the increase in taurine level alongside with GABA can be regarded as components of recovery therapy…

Our findings led us to a conclusion that afobazole administered in a dose of 10 mg/kg to the animals 40 min after modeling of global ischemia restored the impaired balance of excitatory and inhibitory amino acids in the striatum, normalized their content to control values, and activates endogenous taurine-dependent neuroprotection system…

Anxiolytic agent afobazole (10 mg/kg intraperitoneally) 24 h after ischemia restores impaired balance of excitatory and inhibitory amino acids in the striatum of mongrel rats, normalizes their content to control levels, and activates endogenous taurine-dependent system of neuroprotection.
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You should administer this cocktail concomitently with the BENZO tapering.

Further to this you might like to try adding PIRACETAM at a dosage of 5 GRAMS TID (total 15g daily)

Thanks for clearing that up. I'm a chemistry student so I have the habit of trying to predict the SARs myself by looking at the structures. Doesn't always work out too well lol. Both of those molecules are GABA analogues so I assumed they mimic the neurotransmitter.

No worries. I come up against this time and time again. I wish they'd RENAME those two drugs! Lol!

Withdrawals from downers can be pretty horrific, the more knowledge we attain, the better we'll be able to deal with them.

Agreed

When I get my masters in a chemistry/pharmacology related field, I want to research ibogaine analogues because I suspect that molecule may propel us into a new paradigm in which drug addiction isn't the seemingly inescapable nightmare that it is for many people...

I happen to have 3 grams of pure IBOGAINE HCl sitting on my desk in front of me as I type this

Ah shit, you're right. Now I'm worried. Hopefully phenibut has very low GABA(A) activity. I have some xanax coming in a few days but all I have right now is phenibut. I can get some diazepam from a doctor if I really need to. My plan is to just use the xanax to sleep for a week, then taper down off it.

I think ALPRAZOLAM (XANAX) will do fine for the BENZO TAPERING process

Edited by ScienceGuy, 10 July 2012 - 11:48 AM.

[mycotheologist]

Thanks a lot for the info ScienceGuy. This is gonna help me immensely. Before reading this thread, I had a limited number of tricks up my sleeve for dealing with GABAergic withdrawals. I ordered some bacopa monneira extract. I'm looking into afobazole, very interesting. It even has neuroprotective properties. I use magnesium regularly but I've yet to try the l-threonate salt. I should have came to this forum years ago, I've learned more browsing 3 or 4 threads here than I do browsing dozens of threads on other forums.

[mycotheologist]

quamquam1: Have you considered ibogaine? I read reports from people claiming that a single high dose of ibogaine completely cured all their protracted benzo w/d symptoms. Also, I recommend taking a look at forums.ayahuasca.com I have read reports that ayahuasca does the same thing. Heres a thread I started there:
http://forums.ayahua...p?f=17&p=222976

[hooter]

I watched all of xena but when it was over i suddenly got heroine withdrawal.. *sigh*

[Rior]

quamquam1: Have you considered ibogaine? I read reports from people claiming that a single high dose of ibogaine completely cured all their protracted benzo w/d symptoms. Also, I recommend taking a look at forums.ayahuasca.comI have read reports that ayahuasca does the same thing. Heres a thread I started there:
http://forums.ayahua...p?f=17&p=222976

That's because your mind is thrown so far into another world that withdrawals don't exist anymore. Seriously though, Ayahuasca or ibogaine for withdrawal alleviation is a terrible idea unless the person reeeeeeeeally knows what they're getting themselves into. It's more about the spiritual journey than the alleviation of withdrawals.

[ScienceGuy]

quamquam1: Have you considered ibogaine? I read reports from people claiming that a single high dose of ibogaine completely cured all their protracted benzo w/d symptoms. Also, I recommend taking a look at forums.ayahuasca.comI have read reports that ayahuasca does the same thing. Heres a thread I started there:
http://forums.ayahua...p?f=17&p=222976

Mycotheologist,

Whilst you are quite correct regarding the ANTI-ADDICTION properties of IBOGAINE, please kindly note that you need to be very careful recommending its usage to people willy-nilly, since there are some extremely important precautions and clinical supervision that absolutely must be followed when using IBOGAINE, due to its possible effects on the CARDIOVASCULAR SYSTEM. As such, nobody should take IBOGAINE without undergoing both.

In short, you need to undergo a number of medical tests prior to taking it, including ECG as well as LIVER and RENAL FUNCTION blood tests, and then when you take it, it is vital that you do so whilst being supervised by someone who is medically trained. To do otherwise will quite literally put you at serious risk. So, I reiterate, unless you are able to undergo IBOGAINE treatment following the correct protocol and precautions you are strongly advised NOT to even consider taking it.

Edited by ScienceGuy, 11 July 2012 - 05:06 PM.

[hooter]

Scienceguy, what do you think about tianeptine in this respect?

[ScienceGuy]

Scienceguy, what do you think about tianeptine in this respect?

Hi Hooter,

TIANEPTINE is safe to take without the precautions necessary when taking IBOGAINE; however, it does have a number of SIDE EFFECTS that you should watch out for, the most common of which appear to include FATIGUE, DEPRESSION and MOOD SWINGS; some people experience some of these, whilst others not at all

P.S. I love your new(ish) avatar comprising bloke covered in CATS

Edited by ScienceGuy, 12 July 2012 - 08:47 AM.

[Rior]

Scienceguy, what do you think about tianeptine in this respect?

Hi Hooter,

TIANEPTINE is safe to take without the precautions necessary when taking IBOGAINE; however, it does have a number of SIDE EFFECTS that you should watch out for, the most common of which appear to include FATIGUE, DEPRESSION and MOOD SWINGS; some people experience some of these, whilst others not at all

P.S. I love your new(ish) avatar comprising bloke covered in CATS

I would also like to bring up working memory problems as possible issues with tianeptine. I work as a server right now in college and found myself unable to remember peoples orders 20-30 seconds later while taking tianeptine 3-5 times a day. As soon as I stopped, my working memory came back fully. I've heard others say it helps their memory, so perhaps it's entirely related to individual physiology. That said, I've also read of its impacts on the nitric oxide system (I believe it acts as an inhibitor in some fashion, but it's been almost a year since I read the study), which has implications in the formation of short term/working memory.

If it's working well for you though, congrats, tianeptine seems great otherwise. My girlfriend and I both had odd memory issues on it.

[protoject]

I f*kn hate tianeptine.. dont really know what all the buzz is about.. i swear it made me more depressed and brain fogged

[mycotheologist]

ScienceGuy: I quit phenibut after 2 weeks of daily use and again, my experience indicates that phenibut has minimal GABA_a activity because I have been taking 0.5mg of alprazolam at night to sleep, then I feel fine for the whole following day. If I had tolerance to the xanax, I would need far more than 0.5mg to get to sleep, considering all the GABA_b downregulation I'm recovering from. On top of that, I would need to keep redosing every 6 hours of so the next day. I may even be able to drop my dosage down to 0.25mg. I actually feel pretty good during the day, I'm a bit groggy in the mornings but thats about it. I have done this once before and when I stopped taking the benzo (diazepam) after around 6 days, there was no acute withdrawal at all. I have never been really addicted to a benzo so I can't say if it works the other way around but I've heard people claim that phenibut masks acute benzo withdrawals. You provide brilliant info but I think you have it wrong when say its best to steer clear of GABA_b agonists when recovering from GABA_a addiction. They allow you to safely and even comfortably get through acute withdrawal after quitting cold turkey. However, I'd say it only works for mild withdrawals, people heavily addicted would probably be better off tapering down first.

[protoject]

ScienceGuy: I quit phenibut after 2 weeks of daily use and again, my experience indicates that phenibut has minimal GABA_a activity because I have been taking 0.5mg of alprazolam at night to sleep, then I feel fine for the whole following day. If I had tolerance to the xanax, I would need far more than 0.5mg to get to sleep, considering all the GABA_b downregulation I'm recovering from. On top of that, I would need to keep redosing every 6 hours of so the next day. I may even be able to drop my dosage down to 0.25mg. I actually feel pretty good during the day, I'm a bit groggy in the mornings but thats about it. I have done this once before and when I stopped taking the benzo (diazepam) after around 6 days, there was no acute withdrawal at all. I have never been really addicted to a benzo so I can't say if it works the other way around but I've heard people claim that phenibut masks acute benzo withdrawals. You provide brilliant info but I think you have it wrong when say its best to steer clear of GABA_b agonists when recovering from GABA_a addiction. They allow you to safely and even comfortably get through acute withdrawal after quitting cold turkey. However, I'd say it only works for mild withdrawals, people heavily addicted would probably be better off tapering down first.

Yeah but then you are just substituting one drug addiction for another whether they have cross tolerance or not. Also I am curious, are benzodiazepine drugs completely selective for gaba-A receptors or is there also some agonism of Gaba-B? Can't remember

[mycotheologist]

Yeah but then you are just substituting one drug addiction for another whether they have cross tolerance or not. Also I am curious, are benzodiazepine drugs completely selective for gaba-A receptors or is there also some agonism of Gaba-B? Can't remember

You have to take alprazolam for at least 3 weeks to get addicted. Benzos are extremely selective towards GABA_a if I'm not mistaken. Phenibut has some GABA_a activity but its clearly very low. Baclofen is even more selective towards GABA_b.

EDIT: I forgot, the tabs I have are 0.5mg, not 0.25mg so I've been taking 1mg of xanax per day. I end up highly sedated though, the dosage is clearly more than I need to sleep. Tonight, I'm going to half the dosage. Tomorrow I'm gonna see if I can sleep without it. There are many reasons why this is better than quitting cold turkey. By quitting a GABAergic cold turkey, you flood your brain with glutamate which causes brain damage. With mild withdrawals, I don't think seizures are an issue but glutamate excitotoxicity probably still is to some degree. Another reason is that like this, the withdrawal is comfortable, rather than agonising. Like I said, I have done this before. When I quit the benzo, there was no acute withdrawal. There were some PAWS though.

I'll keep you updated on how this works out anyway. I need to get off everything and get back to baseline ASAP so I can try out new things. My last dose of phenibut was on Tuesday night, now its Friday night. I just took 0.75mg of xanax, I'll probably take 0.5mg tomorrow night and then I'm gonna jump off and see what happens. The first time I did this, I stayed on the xanax for a week then took a few days worth of valium and I was able to sleep every night after that.

Edited by mycotheologist, 13 July 2012 - 08:57 PM.

[ScienceGuy]

ScienceGuy: I quit phenibut after 2 weeks of daily use and again, my experience indicates that phenibut has minimal GABA_a activity because I have been taking 0.5mg of alprazolam at night to sleep, then I feel fine for the whole following day. If I had tolerance to the xanax, I would need far more than 0.5mg to get to sleep, considering all the GABA_b downregulation I'm recovering from. On top of that, I would need to keep redosing every 6 hours of so the next day. I may even be able to drop my dosage down to 0.25mg. I actually feel pretty good during the day, I'm a bit groggy in the mornings but thats about it. I have done this once before and when I stopped taking the benzo (diazepam) after around 6 days, there was no acute withdrawal at all. I have never been really addicted to a benzo so I can't say if it works the other way around but I've heard people claim that phenibut masks acute benzo withdrawals. You provide brilliant info but I think you have it wrong when say its best to steer clear of GABA_b agonists when recovering from GABA_a addiction. They allow you to safely and even comfortably get through acute withdrawal after quitting cold turkey. However, I'd say it only works for mild withdrawals, people heavily addicted would probably be better off tapering down first.

Hi mycotheologist,

With the utmost respect, you are treading on very dangerous ground. Addiction to GABA RECEPTOR AGONISTS is a very serious and real problem indeed and it is crucial that it is properly treated.

The indisputable fact is that substances that have an affinity for one GABA RECEPTOR almost always will to an extent also have an affinity for the others too. Even in the instances wherein this affinity is weaker it still exists; and hence taking said substance for treating a relevant ADDICTION or WITHDRAWAL is ill advised, and especially so in the instance wherein there are other substances that can be used to effectively treat the ADDICTION or WITHDRAWAL which do not in any regard have an affinity for binding to those same receptors.

Furthermore, you simply cannot take your interpretation of your own personal anecdotal experience in taking PHENIBUT and BENZOS and make the definitive conclusions that you have made, such as: "phenibut has minimal GABA_a activity" and "I think you have it wrong when say its best to steer clear of GABA_b agonists when recovering from GABA_a addiction. They allow you to safely and even comfortably get through acute withdrawal after quitting cold turkey. However, I'd say it only works for mild withdrawals, people heavily addicted would probably be better off tapering down first."

Any such conclusions can only be inferred from substantiated scientific evidence; and currently the science unfortunately does not agree with you.

Take your view on using BACLOFEN for treating ALCOHOLISM for example, as it stands the scientific evidence regarding this is conflicting at best and as such it would not be recommended until this situation changes. See this meta-analysis report published very recently (only 6 months ago):

Tidsskr Nor Laegeforen. 2011 Nov 1;131(21):2132-3.
[Baclofen for alcohol addiction].

[Article in Norwegian]
Helland A, Bramness JG.

Source
Avdeling for klinisk farmakologi, St. Olavs hospital, Norway. arne.helland@legemidler.no

Abstract
Baclofen is approved for muscle spasms and cerebral spasticity. Several studies have recently investigated the use of baclofen for alcohol withdrawal symptoms and as an abstinence-promoting agent in alcohol-dependent subjects. The evidence is too weak to recommend baclofen for alcohol withdrawal, and drugs with better documentation such as benzodiazepines and carbamazepine should be preferred for this indication. The evidence for the use of baclofen to prevent relapse to drinking in alcohol dependence is somewhat conflicting, but the drug could be considered as a therapeutic option in case of conservative measures and approved drugs such as disulfiram and acamprosate having insufficient effect. Despite enthusiastic appraisal in case reports, the use of baclofen in high doses to suppress alcohol craving cannot be recommended due to insufficient evidence. Trials that may resolve this issue are underway.

PMID: 22048211

Hence I reiterate that, in my opinion, when treating ADDICTION or WITHDRAWAL from BENZOS it is best to apply an appropriate TAPERING DOWN protocol of an appropriate BENZO and to avoid any and all other GABA RECEPTOR AGONISTS.

In combination with this other substances should be employed that are not GABA RECEPTOR AGONISTS, but which will assist in the recovery process, whether it be to alleviate the WITHDRAWAL SYMPTOMS or to UPREGULATE the GABA SYSTEM.

Edited by ScienceGuy, 14 July 2012 - 08:02 AM.

[ScienceGuy]

You have to take alprazolam for at least 3 weeks to get addicted...

Again, please be careful to avoid making such sweeping, bold statements without the proper scientific substantiation; whilst it is true that most people will need to take ALPRAZOLAM for a prolonged period to become addicted, some individuals (e.g. those with addictive personalities) may become addicted significantly quicker. In other words, the duration it takes to become addicted will depend upon the individual; and hence your statement is an overgeneralisation.

I hope you don't take me correct you in this regard the wrong way. BENZO ADDICTION is a very serious issue and it is vital that all the information put out there regarding it is factually accurate and correct. Hope you understand.

Edited by ScienceGuy, 14 July 2012 - 08:08 AM.

[mycotheologist]

I see what you're saying but you're misinterpreting what I'm saying. What I'm saying is that in my experience benzos can be used to get through the acute phenibut withdrawal comfortably, then when you quit the benzo after a week or so, there is no acute withdrawal. I've done this before but I don't have enough experience to come to any definite conclusions, I'll see how it goes this time and report back. The prospect of alprazolam addiction scares me so I'm planning on jumping off early (tomorrow) and then use all the information you've provided me to treat the symptoms safetly, without GABAergics. I have l-theanine and bacopa coming in the post. Using the xanax for a few days will give me a good head start but I need to get off all these GABAergics ASAP so I can start experimenting with safer, non addictive solutions (since I've joined this forum, I have a long list of things to try).

What I'm worried about is the PAWS I may have to face when I quit everything. I had them last time I quit and they lasted weeks. You've provided a wealth of info in your thread and this one about how to treat the PAWS safely, without GABAergics though so I'm a lot more optimistic about it now. Thanks a lot!

Edited by mycotheologist, 14 July 2012 - 01:31 PM.

[Raza]

Hey scienceguy. Some questions.

- Kava is clearly a GABAergic, but a lot of people report sensitization from repeated use, instead of the tolerance and withdrawals you would expect from an agonist. It's supposed to potentiate GABA A signals somewhere downstream, rather than (or possibly as well as) through classical agonism. Have you really looked to get the full story down on this one?

- How is increasing GABA production through Theanine different from, say, inhibiting gabatransaminase with regards to gaba receptor downregulation? Doesn't anything that increases gaba agonism cause downregulation all the same?

- Why is it necessary to taper benzo use with a benzo, rather than an ordinary gaba-a agonist like valerian? One is a multiplier while the other is additive, but the effect should be the same so long as you get the potency and duration right.

- I don't agree that Bacopa upregulates GABA receptors. The study you quoted monitored effects on rats deficient in GABA receptors due to epilepsy, not prolonged use of GABAergics, and concludes that Bacopa (being an anticolvulsant) prevented (not reversed) a reduction in GABA receptor density caused by repeated seizures. This would not work on anyone suffering from reduced GABA receptors for any other reason, and in fact it seems perfectly probable that a GABA-agonist would have the same effect on epileptic rats, with the benefit from preventing seizures outweighing ordinary downregulation. This explanation is supported by the fact that treatment with Bacopa only increased GABA receptor density in epileptic rats to near control levels, consistent to what you'd see if weak downregulation from a GABA agonist outweighted severe damage by seizures.

That said, Bacopa is a 5-HT1A agonist, which explains anxiolytic properties that exceed whatever gabaergic effect it may or may not have.

Edited by Raza, 14 July 2012 - 03:29 PM.

[Raza]

An (admittedly old) study reporting upregulation of GABA A receptors in response to Kava extract:

http://www.ncbi.nlm..../pubmed/7701051

Abstract

Regional differences in the modulation of [3H] muscimol binding to GABAA receptor complexes by kavapyrones, compounds of the rhizome of the plant Piper methysticum which possess sedative activity, were demonstrated using membrane fractions obtained from target brain centers of kavapyrone action: hippocampus (HIP), amygdala (AMY) and medulla oblongata (MED), and from brain centers outside the main kavapyrone effects as frontal cortex (FC) and cerebellum (CER). The kava extract enhanced the binding of [3H] muscimol in a concentration-dependent manner with maximal potentiation of 358% over control in HIP followed by AMY and MED (main target brain centers). Minimal stimulation was observed in CER followed by FC. In contrast, apart from CER, the potency of kavapyrones was similar in the brain areas investigated with EC50 values ranging between 200 and 300 microM kavapyrones. Scatchard analysis revealed that the observed effects of kavapyrones were due to an increase in the number of binding sites (Bmax), rather than to a change in affinity. At a kavapyrone concentration of 500 microM the order of enhancement in Bmax was HIP = AMY > MED > FC > CER. When kavapyrones are included together with pentobarbital or HPO the two classes of compounds produced a more than additive, i.e., synergetic effect on [3H] muscimol binding. Our findings suggest that one way kavapyrones might mediate sedative effects in vivo is through effects on GABAA receptor binding.

And a reference to another one:

Kavalactones increase GABA receptor density in specific areas of rodent brain (especially hippocampus and amygdala) suggesting GABA-a receptor mediation of the sedative effects of kava, although earlier studies did not find GABA or benzodiazepine receptor binding. German EEG studies have confirmed the limbic structures, especially the amygdylar complex, mediate the sedative effects of kava
(Holm E, et al. Arzneimittelforschung 1991 Jul;41(7):673-683.)

Edited by Raza, 17 July 2012 - 08:24 PM.

[c60tester]

If you really want to reserve the effects benzodiazapines do to the brain my guess would be to take drugs that have the opposite effects in the brain.
Inverse agonists like α5IA, L-655,708, and DMCM do this but some have adverse effects like anxiety, convulsions, and renal toxicity.

Maybe the ones that create anxiety could lessen anxiety in the long run in the same way you get anxiety from taking benzos for a while and them getting off them.

[mycotheologist]

ScienceGuy: I took alprazolam for exactly 1 week after quitting phenibut. Its been 2 days since my last dose of alprazolam and I'm back to normal. No withdrawal. I haven't even missed a nights sleep. On the 2nd day after stopping, I was depressed and anxious for the whole day but by nighttime, I felt fine. Now its day 3 and I feel good. I said it before and I'll say it again, phenibut exhibits VERY LOW cross tolerance with benzos so these 2 classes of drugs can be safely used to help circumvent each others acute withdrawal symptoms. Its nothing at all like treating an alcohol withdrawal with a few shots of vodka, its more like using gabapentin during an opioid withdrawal. I know you mean well but by following your advice to avoid ALL GABAergic drugs, people would be forcing themselves to endure completely unnecessary suffering. I've got off phenibut twice now with benzos and once with z drugs without needing to taper. This approach works. Theory is founded upon empirical observation, not the other way around. People need to know about this because it can save one a massive amount of suffering. I quit cold turkey from phenibut after a 2 week binge in the past and I couldn't sleep for 5 days straight and felt like crap for the duration of the withdrawal. This time I felt good the whole time.

Edited by mycotheologist, 20 July 2012 - 09:08 AM.

[mycotheologist]

I should mention though that while I feel fine if I take nothing, opioids give me real bad anxiety about 4 hours after I take them. Its interesting because I feel great for the first couple of hours then I gradually start getting more anxious. After reading a bit about opioid pharmacology I think I have a solid explanation. Opioids prevent GABA from being released so after I take them, my brain starts outputting less GABA and the levels of GABA in my brain gradually decrease. I've been taking dihydrocodeine which usually lasts around 6 hours and the anxiety is at its worst at around 6 hours. As the drug wears off, I start feeling good again as my GABA levels increase. Interesting stuff. I took some bacopa and gotu kola capsules but they didn't help at all. I didn't take any l-theanine so as not to further increase the amount of dopamine. I ordered some picamilon today so I'm looking forward to experimenting with it to see how it alleviates these mild protracted w/d symptoms.

[madamshome]

True, alcohol, if I'm not mistaken, binds primarily to GABA_a receptors but it clearly has some affinity to GABA_b receptors too since it exhibits cross tolerance with GHB. However, baclofen is the GABAergic of choice for managing alcohol withdrawal symptoms since it exhibits relatively low cross tolerance.

The fact that BACLOFEN is the GABAergic of choice for managing ALCOHOL WITHDRAWAL symptoms does not mean it is the best choice of substance for managing alcohol withdrawal symptoms.

METHADONE is a drug of choice for treating HEROINE WITHDRAWAL but that's not the best choice either; and personally I strongly recommend against its usage as one is simply replacing one addiction with another.

I read all your posts in this thread, the one you mentioned which I'm going to try out on this phenibut w/d is l-theanine. I like the fact that it has some glutamate antagonist properties because it should help protect against brain damage (caused by glutamate excitotoxicity). So far, the only non GABAergics I have tried during GABAergic withdrawals are amphetamines and opioids. Amphetamines was a huge mistake (not surprising lol). Opioids seem to make things worse too.

See how you get on with THEANINE. In my experience it is highly unpredictable with regards to how each person responds to it. For some individuals it can be a magic bullet and find it is wonderful; but others react badly to it, in which case it would make your withdrawal symptoms worse. You will need to ascertain whether you are a positive or negative responder to it.

Further to this I recommend that you consider self-adminstering the following cocktail of substances:

1) MAGNESIUM - For someone in your situtation I'd recommend a combination of MAGNESIUM L-THREONATE taken PER ORALLY during the day (it may assist your studies too ) plus MAGNESIUM SULPHATE administered TRANSDERMALLY via adding 1-2 cups to a HOT BATH into which you soak for at least 12 MINUTES DAILY. MAGNESIUM is not a magic bullet, but it is a very effective and useful tool in treatiing BENZO WITHDRAWAL. Incidentally, please kindly note that MAGNESIUM's primary mechanism of action as ANXIOLYTIC is NMDA RECEPTOR ANTAGONIST so provides the protection against GLUTAMATE NEUROTOXICITY that you seek.

2) BACOPA MONNIERI EXTRACT - to commence UPREGULATION and hence RECOVERY of your GABA SYSTEM. It exerts an ANXIOLYTIC effect so will help with the withdrawal symptoms. READ THIS:

Epilepsy Behav. 2010 Apr;17(4):441-7. Epub 2010 Feb 11.

Behavioral deficit and decreased GABA receptor functional regulation in the cerebellum of epileptic rats: effect of Bacopa monnieri and bacoside A.

Mathew J, Peeyush Kumar T, Khan RS, Paulose CS.

Source
Department of Biotechnology, Molecular Neurobiology and Cell Biology Unit, Centre for Neuroscience, Cochin University of Science and Technology, Kerala, India.

Abstract
In the present study, the effects of Bacopa monnieri and its active component, bacoside A, on motor deficit and alterations of GABA receptor functional regulation in the cerebellum of epileptic rats were investigated. Scatchard analysis of [(3)H]GABA and [(3)H]bicuculline in the cerebellum of epileptic rats revealed a significant decrease in B(max) compared with control. Real-time polymerase chain reaction amplification of GABA(A) receptor subunits-GABA(Aalpha1), GABA(Aalpha5,) and GABA(Adelta)-was downregulated (P<0.001) in the cerebellum of epileptic rats compared with control rats. Epileptic rats exhibit deficits in radial arm and Y-maze performance. Treatment with B. monnieri and bacoside A reversed these changes to near-control levels. Our results suggest that changes in GABAergic activity, motor learning, and memory deficit are induced by the occurrence of repetitive seizures. Treatment with B. monnieri and bacoside A prevents the occurrence of seizures thereby reducing the impairment of GABAergic activity, motor learning, and memory deficit.
PMID: 20153260

----------------------------------------------------------------------------------------------------------------------------------------------

And specifically to reverse the effects of Diazepam on the benzodiazepine pathway:

Psychopharmacology (Berl) 2008 Sep;200(1):27-37. Epub 2008 Jan 13.

Bacopa monniera exerts antiamnesic effect on diazepam-induced anterograde amnesia in mice.

Prabhakar S, Saraf MK, Pandhi P, Anand A.

Source
Department of Neurology, Post Graduate Institute of Medical Education and Research, Sector-12, Chandigarh, 160012, India.

Abstract

RATIONALE:

As Benzodiazepines are known to produce amnesia by involvement of the GABAergic system, we examined Bacopa monniera, an herb known for memory enhancement for reversal of memory deficits caused by diazepam.

OBJECTIVES:

The objective of the study was to study the effect of standardized extract of B. monniera on diazepam-induced amnesia in mice using Morris water maze.

MATERIALS AND METHODS:

We used the rota rod test as a screening measure for muscle incoordination followed by the Morris water maze scale to evaluate the effect of B. monniera on amnesia. The index of acquisition and retrieval was recorded with varying doses of Bacopa.

RESULTS:

The results revealed antiamnesic effects of B. monniera (120 mg kg(-1) oral) on diazepam (1.75 mg kg(-1) intraperitoneal)-induced amnesia. The degree of reversal by Bacopa was significant as it progressively reduced escape latency time when mice treated with diazepam were subjected to acquisition trials.

CONCLUSIONS:

The antiamnesic effects of Bacopa suggest likely a gamma-aminobutyric acid-benzodiazepine pathway possibly affecting long-term potentiation.

PMID: 18193203

3) AFOBAZOLE - This is an effective ANXIOLYTIC that also UPREGULATES the GABA SYSTEM and hence should be especially useful in treating BENZO withdrawal. READ THIS:

Bulletin of Experimental Biology and Medicine, Vol. 151, No. 5, September, 2011 PHARMACOLOGY AND TOXICOLOGY

Effects of Afobazole on the Content of Neurotransmitter Amino Acids in the Striatum in Global Transient Ischemia

V. S. Baykova, I. A. Kadnikov, M. V. Voronin, T. S. Ganshina, A. V. Gnezdilova, A. A. Gorbunov, P. C. Mirzoyan, and S. B. Seredenin

EDITED FROM FULL TEXT:

The objective of this study was to investigate delayed effects of afobazole on the levels of neurotransmitter amino acids in brain structures…

GABA level was significantly decreased in the striatum of ischemic rats. After afobazole administration, GABA level improved and reached the control values recorded in intact animals…

Afobazole administration resulted in restitution of striatal GABA content, which approached the control values; this should promote recovery of neuroprotective systems related to inhibitory influences…

Afobazole administration to ischemic animals resulted in more substantial increase in taurine level in the striatum. Agonistic interaction between afobazole and σ1-receptors, possibly underlies this phenomenon…

Thus, the increase in taurine level alongside with GABA can be regarded as components of recovery therapy…

Our findings led us to a conclusion that afobazole administered in a dose of 10 mg/kg to the animals 40 min after modeling of global ischemia restored the impaired balance of excitatory and inhibitory amino acids in the striatum, normalized their content to control values, and activates endogenous taurine-dependent neuroprotection system…

Anxiolytic agent afobazole (10 mg/kg intraperitoneally) 24 h after ischemia restores impaired balance of excitatory and inhibitory amino acids in the striatum of mongrel rats, normalizes their content to control levels, and activates endogenous taurine-dependent system of neuroprotection.
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------

You should administer this cocktail concomitently with the BENZO tapering.

Further to this you might like to try adding PIRACETAM at a dosage of 5 GRAMS TID (total 15g daily)

Thanks for clearing that up. I'm a chemistry student so I have the habit of trying to predict the SARs myself by looking at the structures. Doesn't always work out too well lol. Both of those molecules are GABA analogues so I assumed they mimic the neurotransmitter.

No worries. I come up against this time and time again. I wish they'd RENAME those two drugs! Lol!

Withdrawals from downers can be pretty horrific, the more knowledge we attain, the better we'll be able to deal with them.

Agreed

When I get my masters in a chemistry/pharmacology related field, I want to research ibogaine analogues because I suspect that molecule may propel us into a new paradigm in which drug addiction isn't the seemingly inescapable nightmare that it is for many people...

I happen to have 3 grams of pure IBOGAINE HCl sitting on my desk in front of me as I type this

Ah shit, you're right. Now I'm worried. Hopefully phenibut has very low GABA(A) activity. I have some xanax coming in a few days but all I have right now is phenibut. I can get some diazepam from a doctor if I really need to. My plan is to just use the xanax to sleep for a week, then taper down off it.

I think ALPRAZOLAM (XANAX) will do fine for the BENZO TAPERING process

[madamshome]

Great info, thanks Scienceguy. I am having a painful & ridiculously long taper from medically prescribed valium, (start dose 5mg, now at 0.75mg, (yes the decimals are in the right place, I seem to be bizarrely sensitive).
On your evidence, I am now trying the bacopa, but hazarding a guess as to how the mouse dose of 120 mg/ kg translates to my 56kg person. I am trialling 750mgs twice daily. Some minor gastric discomfort but otherwise seems positive, (though only day 2, so too early to tell). Any suggestions on dose?

Have also ordered some afobazole but haven't heard from the pharmacy since I WUd payment, so hoping they have not degenerated into scamville.

Thanks for your help & sorry about the red line, can't seem to select it back to black.

Mycotheologist, my casual observation as a masters biochem student, is that you are being a bit rough & ready with your experimental protocol. Too many variables at once & insufficient experiment time. GABA receptors are very very slow to upregulate & as Scienceguy has said, adding more down-regulators will make things worse.

Diazepam has the longest half life of all the benzos & for this reason is regarded as the easiest of the class to taper from. See Dr Ashton's protocol at http://www.benzo.org.uk/manual/ if you are interested.