139 replies to this topic

[quamquam91]

Hello,

I quit taking benzodiazepines cold-turkey (I was abusing many different benzos at once) almost ten months ago.

I already exercise quite frequently (weights and cardio, particularly running), which helps with the anxiety and delusions but not with sleep.

The withdrawal has been debilitating and has shown little sign of letting up. The withdrawal has included:

--Paranoia and the feeling of being punished, among other delusions (never a problem pre-withdrawal)
--The all-consuming feeling that nothing around me is real
--Misery and dejection
--Crippling insomnia and constant night terrors (average of 4-5 hours of sleep a night)
--Thick brain fog and inability to speak or write fluently (even keeping up a conversation can be a challenge)

The withdrawal has come in cycles--a day or two of normality, a day or two of suffering. Lately it's been one or two days of normality for every three or four days of suffering. Very hard to endure.

Yesterday I took Gotu Kola and it cleared all of these symptoms up. I felt like my old self. Better, in fact. Is Gotu Kola safe to use long term? Will I develop the same tolerance to it that got me into trouble with the benzos?

I am also curious about piracetam and bacopa to address the lingering cognitive deficit and the obsessive, delusional thinking.

My knowledge of brain and nervous system chemistry is quite amateur and superficial. I'm hoping somebody with a real depth of knowledge might be able to help me determine how best to address extremely protracted benzo withdrawal.

Edited by quamquam91, 28 January 2012 - 06:59 PM.

[Introspecta]

If I was going through benzo withdrawal I would try using Valerian root, Ashwagandha, Theanine, and Kava Kava to help aid the withdrawals. You may develop tolerance to Gotu kola but will never get into "trouble" with it. Piracetam will help you with focus just make sure you don't mix caffiene with it because it will probably put your withdrawal into hyperdrive. Have you tried anything besides the Gotu Kola for your WD's?

[quamquam91]

So gotu kola won't impede the process of GABA upregulation? (Although I read somewhere that benzos actually upregulate GABA but make it less effective--I get lost pretty easily in the terminology.)

Here's what I've already tried:

For Sleep

Worked, But Made Me Slow the Next Day
Seroquel
Diphenhydramine

Stupefied Me, But No Effect on Sleep
Trazodone
L-theanine
5-htp

No Discernible Effect
Chamomile
Melatonin
Valerian
Magnesium citrate

For Functioning

Restored Full Functioning, But Caused Withdrawal Relapse Afterward
Progesterone
Cannabis (worst possible choice I could have made--followed by a month of paranoia)
Adderall (almost as bad of a choice)

Better Mood, Worsened Brain Fog
Inositol
The ketogenic diet (lasted about a week before the exhaustion and brain fog got too bad)
Ginseng

Sometimes "Just Right," Sometimes Tweaked-Out
Caffeine

Very Uncomfortable
B-complex

Edited by quamquam91, 29 January 2012 - 02:25 AM.

[Introspecta]

What benzo were you on and for how long?

[quamquam91]

Diazepam, lorazepam, clonazepam, alprazolam. And also zolpidem and alcohol.

Daily usage for only a couple of months before I quit cold-turkey. Leading up to that, intermittent usage (almost daily some weeks, none at all other weeks) for two and a half years.

I was eighteen when I started. I just liked smoothing out bad trips and weed freak-outs. I didn't have a fucking clue.

Periodic binges, e.g. 2+mg alprazolam or 40mg diazepam or, once, 100mg zolpidem. Usual dosage might be .5-1mg alprazolam or its equivalent (1-2mg lorazepam, .5-1mg clonazepam, 10-20mg diazepam)

Since quitting, 10 months of suffering like I could never have imagined.

I'm getting better. When the brain fog's not present, my thinking's becoming fleshed-out again (rather than flattened and plodding). I'm developing a better social awareness (body language, etc.) than even pre-withdrawal.

But the paranoia and delusions and derealization seep in. And the insomnia, my God! Describing these phenomena in clinical terms robs them of their anguish ...

Edited by quamquam91, 29 January 2012 - 06:02 AM.

[ScienceGuy]

If I was going through benzo withdrawal I would try using Valerian root...

The mechanism of action of BENZODIAZEPINES is that of GABA RECEPTOR AGONISM

Hence, you want to AVOID ALL GABA RECEPTOR AGONISTS if going through BENZO WITHDRAWAL

Therefore, you in fact DO NOT want to use VALERIAN, since VALERIAN IS A GABA RECEPTOR AGONIST

The only exception to this is if you are following a TAPERING-DOWN PROTOCOL to wean yourself off of the Benzos (WHICH IS STRONGLY ADVISED), in which case you should switch to using a Benzo with a short half-life and use that for the tapering-down process; in which case you STILL would not want to use VALERIAN.

See the following:

Neuropharmacology. 2007 Jul;53(1):178-87. Epub 2007 May 13.

Valerenic acid [from Valerian] potentiates and inhibits GABA(A) receptors: molecular mechanism and subunit specificity.

Khom S, Baburin I, Timin E, Hohaus A, Trauner G, Kopp B, Hering S.

Source
Department of Pharmacology and Toxicology, University of Vienna, Althanstrasse 14, A-1090 Vienna, Austria.

Abstract
Valerian is a commonly used herbal medicinal product for the treatment of anxiety and insomnia. Here we report the stimulation of chloride currents through GABA(A) receptors (I(GABA)) by valerenic acid (VA), a constituent of Valerian. To analyse the molecular basis of VA action, we expressed GABA(A) receptors with 13 different subunit compositions in Xenopus oocytes and measured I(GABA) using the two-microelectrode voltage-clamp technique. We report a subtype-dependent stimulation of I(GABA) by VA. Only channels incorporating beta(2) or beta(3) subunits were stimulated by VA. Replacing beta(2/3) by beta(1) drastically reduced the sensitivity of the resulting GABA(A) channels. The stimulatory effect of VA on alpha(1)beta(2) receptors was substantially reduced by the point mutation beta(2N265S) (known to inhibit loreclezole action). Mutating the corresponding residue of beta(1) (beta(1S290N)) induced VA sensitivity in alpha(1)beta(1S290N) comparable to alpha(1)beta(2) receptors. Modulation of I(GABA) was not significantly dependent on incorporation of alpha(1), alpha(2), alpha(3) or alpha(5) subunits. VA displayed a significantly lower efficiency on channels incorporating alpha(4) subunits. I(GABA) modulation by VA was not gamma subunit dependent and not inhibited by flumazenil (1 microM). VA shifted the GABA concentration-effect curve towards lower GABA concentrations and elicited substantial currents through GABA(A) channels at > or = 30 microM. At higher concentrations (> or = 100 microM), VA and acetoxy-VA inhibit I(GABA). A possible open channel block mechanism is discussed. In summary, VA was identified as a subunit specific allosteric modulator of GABA(A) receptors that is likely to interact with the loreclezole binding pocket.
PMID:17585957

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The Gamma-Aminobutyric Acidergic Effects of Valerian and Valerenic Acid on Rat Brainstem Neuronal Activity [EDITED FULL TEXT]

• Chun-Su Yuan, MD PhD
• Sangeeta Mehendale, MD PhD
• Yingping Xiao, PhD
• Han H. Aung, MD
• Jing-Tian Xie, MD and
• Michael K. Ang-Lee, MD

Author Affiliations

• *Department of Anesthesia & Critical Care,
• Tang Center for Herbal Medicine Research, and
• Committee on Clinical Pharmacology and Pharmacogenomics, Pritzker School of Medicine, University of Chicago, Chicago, Illinois

Abstract
Valerian is a medicinal herb that produces anxiolytic and sedative effects. It was suggested that valerian acts via gamma-aminobutyric acid (GABA)ergic mechanisms. Previous studies showed binding of valerian extract to GABA receptors, but the functional effect of the binding has not been demonstrated. In this study we evaluated the GABAergic effect of valerian extract and one of its major constituents, valerenic acid, on brainstem neuronal activity in an in vitro neonatal rat brainstem preparation. We first observed that muscimol, a GABA_A receptor agonist, decreased the firing rate in most brainstem neurons in a concentration-related fashion; 30 μM produced a 38.9% ± 3.0% (mean ± se) inhibition compared with control values (P < 0.01; 50% inhibitory concentration [IC₅₀], 2.0 ± 0.1 μM). This effect was antagonized by bicuculline (10 μM), a GABA_A antagonist. Then we showed that valerian extract 3 mg/mL induced a 29.6% ± 5.1% inhibition with an IC₅₀ of 240 ± 18.7 μg/mL, whereas 100 μM valerenic acid induced a 22.2% ± 3.4% inhibition with an IC₅₀ of 23 ± 2.6 μM (both P < 0.01). Bicuculline antagonized the inhibitory effects of both the valerian extract and valerenic acid. In addition, pretreatment with valerian extract or valerenic acid decreased the brainstem inhibitory effects produced by muscimol (both P < 0.05), suggesting that these compounds play an important role in the regulation of GABAergic activity. Data from this study suggest that the pharmacological effects of valerian extract and valerenic acid are mediated through modulation of GABA_A receptor function. Thus, valerian may potentiate the sedative effects of anesthetics and other medications that act on GABA receptors, and presurgical valerian use may cause a valerian-anesthetic interaction…

Discussion
…In this study, we demonstrated that treatment with valerian extract or valerenic acid caused an inhibitory effect on muscimol-sensitive NTS neurons in an in vitro brainstem preparation. We also observed that the inhibitory activity of both valerian extract and valerenic acid was induced via GABA_A, but not GABA_B, receptors. Previous studies showed the binding of valerian extract to GABA_A receptors in rat cortical membrane preparation. We observed the neuropharmacological effect of GABA_A activity in our experiment. The GABA agonistic activity of valerian and its positive modulation of GABA_A receptors could partly explain valerian’s antianxiety and sedative effects.
The dose-dependent inhibition of discharge frequency in muscimol-sensitive neurons by valerian extract suggests a GABA_A agonistic activity. This activity could be mediated either by direct receptor action or by increasing the availability of GABA. It has been shown that valerian extract, aqueous or hydroalcoholic, contained GABA and other amino acids that could displace labeled muscimol, suggesting that specific constituents of valerian extract can directly bind to GABA_A receptors. The GABA content of valerian extract could also be responsible for the stimulated release and reuptake of GABA. This could be an indirect mechanism of GABA agonistic activity of valerian extract…
…Our data suggest that the pharmacological effects of valerian extract and valerenic acid are mediated through GABAergic activity. This is also supported by a case report in which valerian withdrawal mimicked an acute benzodiazepine withdrawal syndrome…

Edited by ScienceGuy, 29 January 2012 - 03:59 PM.

[ScienceGuy]

If I was going through benzo withdrawal I would try using... Kava Kava

KAVA KAVA is also a GABA RECEPTOR AGONIST

Therefore, you DO NOT want to take KAVA KAVA if going through BENZO WITHDRAWAL.

Also, the possible HEPATOTOXICITY associated with KAVA use is another reason to steer clear.

See the following:

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

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

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.
PMID: 11458444

[ScienceGuy]

If I was going through benzo withdrawal I would try using... Ashwagandha

ASHWAGHANDHA has been demonstrated to possess GABA-MIMETIC and hence GABA RECEPTOR AGONISM activty.

Therefore, I am afraid that you also DO NOT want to take ASHWAGHANDHA if going through BENZO WITHDRAWAL.

See the following:

Phytother Res. 2010 Aug;24(8):1147-50.

The methanolic extract of Withania somnifera ACTS on GABAA receptors in gonadotropin releasing hormone (GnRH) neurons in mice.

Bhattarai JP, Ah Park S, Han SK.

Source

Department of Oral Physiology and BK21 program, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju, 561-756, Republic of Korea.

Abstract
The effect of the methanol extract of Withania somnifera (mWS) on the gonadotropin releasing hormone (GnRH) neuron was examined in juvenile mice using the whole cell patch clamp technique. GnRH neurons are the fundamental regulators of the pulsatile release of GnRH needed for puberty and fertility. GnRH neurons were depolarized by bath application of the mWS (400 ng/microl) under the condition of a high Cl(-) pipette solution in current clamp mode. In voltage clamp mode, mWS induced reproducible inward currents (31.7 +/- 5.51 pA, n = 14). The mWS-induced inward currents persisted in the presence of tetrodotoxin (TTX, 0.5 microM), but were suppressed by bicuculline methiodide (BMI, 20 microM), a GABA(A) receptor antagonist. These results show that mWS affects the neuronal activities by mediating the GABA(A) receptor, which suggests that WS contains an ingredient with possible GABAmimetic activity.

PMID: 20044800

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Indian J Exp Biol. 2008 Jun;46(6):465-9.

Effect of Withania somnifera Dunal root extract against pentylenetetrazol seizure threshold in mice: possible involvement of GABAergic system.

Kulkarni SK, Akula KK, Dhir A.

Source
Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160 014, India. skpu@yahoo.com

Abstract
Withania somnifera (ashwagandha) is a widely used herb in the Ayurvedic system of medicine. The objective of the present study was to elucidate the effect of W. somnifera root extract (Ws) alone or in combination with exogenous gamma-amino butyric acid (GABA), a GABA receptor agonist or with diazepam, a GABA receptor modulator against pentylenetetrazol (PTZ, iv) seizure threshold in mice. Minimal dose of PTZ (iv, mg/kg) needed to induce different phases (myoclonic jerks, generalized clonus and tonic extension) of convulsions were recorded as an index of seizure threshold. Ws (100 or 200 mg/kg, po) increased the PTZ seizure threshold for the onset of tonic extension phase whereas a lower dose (50 mg/kg, po) did not show any effect on the seizure threshold. Co-administration of a sub-effective dose of Ws (50 mg/kg, po) with a sub-protective dose of either GABA (25 mg/kg, ip) or diazepam (0.5 mg/kg, ip) increased the seizure threshold. The results suggested that the anticonvulsant effect of W. somnifera against PTZ seizure threshold paradigm involved the GABAAergic modulation.

PMID: 18697606

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

Indian J Med Res. 1991 Aug;94:312-5.

Pharmacological effects of Withania somnifera root extract on GABAA receptor complex.

Mehta AK, Binkley P, Gandhi SS, Ticku MK

Source
Department of Pharmacology, University of Texas Health Science Center.

Abstract
A methanolic extract of W. somnifera root inhibited the specific binding of [3H]GABA and [35S]TBPS, and enhanced the binding of [3H]flunitrazepam to their putative receptor sites. The extract (5 micrograms) inhibited [3H]GABA binding by 20 +/- 6 per cent whereas a concentration of 1 mg of the extract produced 100 per cent inhibition. The extract (5-100 micrograms) produced 20 +/- 4 to 91 +/- 16 per cent enhancement of [3H]flunitrazepam binding. In functional studies using 36Cl-influx assay in mammalian spinal cord neurons, W. somnifera root extract increased 36Cl-influx in the absence of GABA. This effect on 36Cl-influx was blocked by bicuculline and picrotoxin; and enhanced by diazepam. These results suggest that the W. somnifera extract contains an ingredient which has a GABA-mimetic activity.

PMID: 1660034

[nupi]

Is it really fully clear that you should not use weaker GABA agonists when going through benzo withdrawal? Might be an effective way to do cross tapering, no?

Also Bacopa seems to have some GABA agonist properties:

http://www.scielo.br/scielo.php?pid=S1984-82502009000400006&script=sci_arttext

Anticonvulsant activity of Bacopa monniera in rodents


Darpan Kaushik^{I, *}; Ashish Tripathi^II; Rashmi Tripathi^II; Madiwalayya Ganachari^III; Suroor Ahmad Khan^I
IF/O Pharmacy, Jamia Hamdard University
^IICollege of Pharmacy, Jakhrota, Agra
^IIIDepartment of Pharmacology, KLE's College of Pharmacy


ABSTRACT
Bacopa monnieri (L), belonging to the Scrophulariaceae family and commonly known as Brahmi, is well known in India for its CNS activity but its neuropharmacological effect has not yet been explored. In the present study, the antiepileptic effects of the plant were investigated. The ethanolic extract of Bacopa monniera was tested for anticonvulsant activity in albino rats, using different convulsive models. The ethanolic extract of leaves produced significant anticonvulsant activity for all the different models studied. The present study shows a probable mechanism of action similar to that of benzodiazepines (GABA agonist). Thus, these results emphasize the need to diversify by using alternative therapeutic approaches pertaining to herbal medicine, where a single easily available plant may provide solutions to several therapeutic challenges, as observed in the anticonvulsant action of ethanolic extract of B. monniera.
Uniterms: Bacopa monniera/pharmacognosy. Anticonvulsant. MES test. PTZ model. Hypoxia model. Strychnine

Edited by nupi, 29 January 2012 - 01:36 PM.

[ScienceGuy]

Is it really fully clear that you should not use weaker GABA agonists when going through benzo withdrawal? Might be an effective way to do cross tapering, no?

Please kindly note my posting above, which answers this for you :

The mechanism of action of BENZODIAZEPINES is that of GABA RECEPTOR AGONISM

Hence, you want to AVOID ALL GABA RECEPTOR AGONISTS if going through BENZO WITHDRAWAL...

The only exception to this is if you are following a TAPERING-DOWN PROTOCOL to wean yourself off of the Benzos (WHICH IS STRONGLY ADVISED), in which case you should switch to using a Benzo with a short half-life and use that for the tapering-down process

Usage of herbal extracts for which the full extent of the interaction with the GABA receptors is unknown is not advised.

ONCE YOU HAVE WEANED YOURSELF DOWN AND HAVE STOPPED TAKING THE BENZOS YOU SHOULD AVOID ALL GABA RECEPTOR AGONISTS. PERIOD.

Edited by ScienceGuy, 29 January 2012 - 03:30 PM.

[ScienceGuy]

Yesterday I took Gotu Kola and it cleared all of these symptoms up. I felt like my old self. Better, in fact. Is Gotu Kola safe to use long term? Will I develop the same tolerance to it that got me into trouble with the benzos?

GOTU KOLA (CENTELLA ASIATICA) is also a GABA RECEPTOR AGONIST and hence should be AVOIDED if in process of recovering form BENZODIAPEZINE WITHDRAWAL

See attached published research study (which incidentally also confirms ASHWAGANDHA being a strong GABA RECEPTOR AGONIST)

Attached Files

•  Ancient-Modern Concordance in Ayurvedic Plants.pdf   462.6KB   30 downloads

[Introspecta]

I don't have time to go through all your studies this moment science but the only reason I suggested that was because they are so weak. I've never heard of anyone having withdrawals from any of those herbs so I wouldn't think it would be a problem. I will check them out though when i get home later. Thanks for posting them

[Introspecta]

I have used all those herbs plus passionflower for phenibut withdrawals and they kept me from having panic attacks and didn't prolong the withdrawals. I realize phenibuts action is a bit different than benzos. I still don't think it will make the situation worse, but I could be wrong.

[ScienceGuy]

OK, since I always like to try to balance NEGATIVITY with POSITIVITY, here's my advise regards WHAT YOU CAN TAKE for effectively and safely treating BENZODIAZEPINE WITHDRAWAL:

1) THEANINE

Firstly, hat's off to joelski28 for suggesting THEANINE!

THEANINE is highly useful in this instance, since it DOES NOT function as a GABA RECEPTOR AGONIST but UPREGULATES THE PRODUCTION OF GABA within the brain, functions as a GLUTAMATE RECEPTOR ANTAGONIST, and enhances ALPHA-WAVE production within the brain.

See the following studies:

J Herb Pharmacother 2006;6(2):21-30.

The neuropharmacology of L-theanine(N-ethyl-L-glutamine): a possible neuroprotective and cognitive enhancing agent.

Nathan PJ, Lu K, Gray M, Oliver C.

Source

Behavioural Neuroscience Laboratory, Department of Physiology, Monash Center for Brain and Behaviour, Monash University, Australia. Nathan@med.monash.edu.au

Abstract
L-theanine (N-ethyl-L-glutamine) or theanine is a major amino acid uniquely found in green tea. L-theanine has been historically reported as a relaxing agent, prompting scientific research on its pharmacology. Animal neurochemistry studies suggest that L-theanine increases brain serotonin, dopamine, GABA levels and has micromolar affinities for AMPA, Kainate and NMDA receptors. In addition has been shown to exert neuroprotective effects in animal models possibly through its antagonistic effects on group 1 metabotrophic glutamate receptors. Behavioural studies in animals suggest improvement in learning and memory. Overall, L-theanine displays a neuropharmacology suggestive of a possible neuroprotective and cognitive enhancing agent and warrants further investigation in animals and humans.
PMID: 17182482

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

AANA J. 2009 Dec;77(6):445-9.

Anxiolytic effects of L-theanine--a component of green tea--when combined with midazolam, in the male Sprague-Dawley rat.

Heese T, Jenkinson J, Love C, Milam R, Perkins L, Adams C, McCall S, Ceremuga TE.

Source
US Army Graduate Program in Anesthesia Nursing, Carl R. Darnell Army Medical Center, Fort Hood, Texas, USA.

Abstract
The purpose of the study was to investigate the anxiolytic effects of L-theanine and its potential interaction with the GABAA receptor in Sprague-Dawley rats. L-theanine is a major component of green tea, which has traditionally been used as an herbal remedy in the treatment of many medical conditions, including anxiety. Herbals and supplements and their potential interactions perioperatively are a concern to anesthetists. Fifty-five rats were divided into 5 groups: control (saline); L-theanine (positive control); flumazenil (a known benzodiazepine receptor antagonist) and L-theanine; and midazolam and L-theanine. The behavioral component of anxiety was evaluated using the elevated plus-maze and calculated by the time spent in the open arm of the maze divided by total time in the maze. Data were analyzed using a 2-tailed multivariate analysis of variance and Sheffé posthoc test. The data suggest that L-theanine does not produce anxiolysis by modulation of the GABAA receptor; however, in combination with midazolam, a synergistic or additive effect was demonstrated by decreased anxiety and both fine and basic motor movements. These data may provide direction for further studies examining L-theanine and its effects on anxiety and motor activity.
PMID: 20108732

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

Clin Neuropharmacol. 2007 Jan-Feb;30(1):25-38.

The deployment of intersensory selective attention: a high-density electrical mapping study of the effects of theanine.

Gomez-Ramirez M, Higgins BA, Rycroft JA, Owen GN, Mahoney J, Shpaner M, Foxe JJ.
Source

Program in Cognitive Neuroscience, Department of Psychology, The City College of the City University of New York, New York, NY, USA.
Abstract

OBJECTIVE:

: Ingestion of the nonproteinic amino acid theanine (5-N-ethylglutamine) has been shown to increase oscillatory brain activity in the so-called alpha band (8-14 Hz) during resting electroencephalographic recordings in humans. Independently, alpha band activity has been shown to be a key component in selective attentional processes. Here, we set out to assess whether theanine would cause modulation of anticipatory alpha activity during selective attentional deployments to stimuli in different sensory modalities, a paradigm in which robust alpha attention effects have previously been established.
METHODS:

: Electrophysiological data from 168 scalp electrode channels were recorded while participants performed a standard intersensory attentional cuing task.
RESULTS:

: As in previous studies, significantly greater alpha band activity was measured over parieto-occipital scalp for attentional deployments to the auditory modality than to the visual modality. Theanine ingestion resulted in a substantial overall decrease in background alpha levels relative to placebo while subjects were actively performing this demanding attention task. Despite this decrease in background alpha activity, attention-related alpha effects were significantly greater for the theanine condition.
CONCLUSION:

: This increase of attention-related anticipatory alpha over the right parieto-occipital scalp suggests that theanine may have a specific effect on the brain's attention circuitry. We conclude that theanine has clear psychoactive properties, and that it represents a potentially interesting, naturally occurring compound for further study, as it relates to the brain's attentional system.
PMID: 17272967



2) BACOPA MONNIERI

Bacopa seems to have some GABA agonist properties:

Anticonvulsant activity of Bacopa monniera in rodents

Darpan Kaushik^{I, *}; Ashish Tripathi^II; Rashmi Tripathi^II; Madiwalayya Ganachari^III; Suroor Ahmad Khan^I
IF/O Pharmacy, Jamia Hamdard University
^IICollege of Pharmacy, Jakhrota, Agra
^IIIDepartment of Pharmacology, KLE's College of Pharmacy

ABSTRACT
Bacopa monnieri (L), belonging to the Scrophulariaceae family and commonly known as Brahmi, is well known in India for its CNS activity but its neuropharmacological effect has not yet been explored. In the present study, the antiepileptic effects of the plant were investigated. The ethanolic extract of Bacopa monniera was tested for anticonvulsant activity in albino rats, using different convulsive models. The ethanolic extract of leaves produced significant anticonvulsant activity for all the different models studied. The present study shows a probable mechanism of action similar to that of benzodiazepines (GABA agonist). Thus, these results emphasize the need to diversify by using alternative therapeutic approaches pertaining to herbal medicine, where a single easily available plant may provide solutions to several therapeutic challenges, as observed in the anticonvulsant action of ethanolic extract of B. monniera.
Uniterms: Bacopa monniera/pharmacognosy. Anticonvulsant. MES test. PTZ model. Hypoxia model. Strychnine

Please kindly note that this study does NOT in fact demonstrate BACOPA to be a GABA AGONIST, since the study did not in any regard evaluate the actual interactions with the GABA RECEPTORS; it merely INFERS THE POSSIBLITY of a GAGAergic mechanism from the facts that:

• BACOPA was shown to potentiate the effects of DIAZEPAM; and
• BACOPA was shown to possess ANTI-CONVULSANT properties.

Please kindly note the following extracted from the FULL TEXT for the particular study:

“BM can lower the dose of diazepam that is requi­red for protection against seizures. This may indicate a GABAergic mechanism as the effect of diazepam was potentiated…”

“The present study shows that the alcoholic extract of Bacopa monniera may function in a similar manner to BZD, given its benzodiazepine-like [anti-convulsant] action, ALTHOUGH THE SPECIFIC RECEPTOR INTERACTIONS WERE NOT EVALUATED. Further evaluation of Bacopa monniera is needed to establish its exact mechanism of action.”

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BACOPA MONNIERI in fact might prove very helpful, since this has been shown in animal studies to upregulate down-regulated GABA receptors:

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) MAGNESIUM

MAGNESIUM might prove to be a very useful adjunct due to its NMDA RECEPTOR ANTAGONISM mechanism of action. See the attached medical publication for details.

I recommend the MALATE form, and total dosage of up to 6.25 grams MAGNESIUM MALATE powder (= 1,000mg Mg) daily in divided doses.


4) TAPERING-DOWN OF GABA RECEPTOR AGONISTS

I feel the need to repeat here the following information:

The mechanism of action of BENZODIAZEPINES is that of GABA RECEPTOR AGONISM

Hence, you want to AVOID ALL GABA RECEPTOR AGONISTS if going through BENZO WITHDRAWAL

The only exception to this is if you are following a TAPERING-DOWN PROTOCOL to wean yourself off of the Benzos (WHICH IS STRONGLY ADVISED), in which case you should switch to using a Benzo with a short half-life and use that for the tapering-down process

Usage of herbal extracts for which the full extent of the interaction with the GABA receptors is unknown is NOT advised for use in the tapering-down process.

ONCE YOU HAVE WEANED YOURSELF DOWN AND HAVE STOPPED TAKING THE BENZOS YOU SHOULD AVOID ALL GABA RECEPTOR AGONISTS. PERIOD.

Attached Files

•  Hippocampal NMDA receptors and anxiety - At the interface.pdf   308.81KB   22 downloads

Edited by ScienceGuy, 29 January 2012 - 03:29 PM.

[hooter]

Word for word what science guy said. AVOID GABA AGONISTS!

When withdrawing from benzodiazepines, do not quit cold turkey. This causes brain damage and can be fatal depending on the dosage and duration of previous intake.

Take bacopa extract and l-theanine. Force yourself to exercise.

Cannabis can be good for benzo withdrawal, as it prevents a lot of the damage. But this is a difficult endeavour and I don't recommend it unless you can buy from a dispensary or grow your own. You would require a high CBD strain such as: R4, harlequinn, etc. Other types could be detrimental.

Recovering from benzos takes an incredibly long time and lots of bacopa and piracetam. Good luck.

Edited by hooter, 29 January 2012 - 03:25 PM.

[quamquam91]

Thanks to ScienceGuy, hooter, and joelski28.

Let me try to distill your suggestions into an action plan.

To recap:

I am many months past the acute stage of benzo withdrawal. However, I have been left with debilitating psychological and cognitive symptoms. The nature of these symptoms is that they seem permanent. I am desperate for lasting relief.

Cannabis is terrible for my benzo withdrawal. It mimics schizophrenia.

I already exercise multiple times most days. It helps. Not enough!

Supplements/herbs/drugs that might help:

• So gotu kola will only protract my withdrawal/recovery? It's been about 48 hours since I took it. Been feeling good since then. Maybe it will last!

• Bacopa might actually hasten recovery? If nothing else, it won't hurt?

• What about piracetam? Also, I saw something about tianeptine in another thread. Any other ideas?

"Incredibly long time" is right.

It's already been ten months! Far too late to taper. (Reinstatement is not an option. Ever.)

Edited by quamquam91, 29 January 2012 - 08:50 PM.

[ScienceGuy]

I am many months past the acute stage of benzo withdrawal... It's already been ten months! Far too late to taper

Tapering is only applicable if you have been and are still taking BENZODIAZEPINES; however, since you ceased taking them 10 months ago that is no longer applicable, and you most certainly should AVOID TAKING ANY ANY ALL GABA RECEPTOR AGONISTS

Cannabis is terrible for my benzo withdrawal...

CANNABIS stimulates a short-term spiking of GABA, but is followed by a subsequent LOWERING OF OVERALL GABA LEVEL in the longer-term, and hence your negative reaction to it is quite understandable. I would avoid it. You want to avoid anything and everything that negatively influences the GABA pathway.

However, I have been left with debilitating psychological and cognitive symptoms. The nature of these symptoms is that they seem permanent.

They are long-lasting, but are almost certainly not permanent. It will get better...

So gotu kola will only protract my withdrawal/recovery? It's been about 48 hours since I took it. Been feeling good since then...

Yes, since GOTU KOLA is a GABA RECEPTOR AGONIST it will prolong your withdrawal and recovery from BENZODIAZEPINES and hence should be avoided. The reason you felt good and relief is because the GOTU KOLA would have been hitting your GABA RECEPTORS...

Bacopa might actually hasten recovery?

YES, IT WILL.

I am desperate for lasting relief... What about piracetam? Also, I saw something about tianeptine in another thread. Any other ideas?

As well as BACOPA, you should use MAGNESIUM; and further to this I recommend that you read up on and consider trying AFOBAZOLE, which is a new ANXIOLYTIC drug which does NOT function via or in any way negatively affect the GABA RECEPTORS.

You can read about AFOBAZOL in this thread here: So I've started Afobazol for my anxiety

You can purchase AFOBAZOL from here: PHARMACY1010 - AFOBAZOL

Reinstatement is not an option. Ever.

You should apply that philosophy to ALL GABA RECEPTOR AGONISTS (i.e. not just BENZODIAZEPINES)

Edited by ScienceGuy, 30 January 2012 - 12:55 PM.

[quamquam91]

Thanks for the response. You do an excellent job of presenting information clearly and concisely, formatted to be easily readable online.

I had no idea cannabis effected GABA! On a related tangent, I've read that caffeine is a GABA (as well as adenosine) antagonist. Is it as essential that I avoid GABA antagonists as it is that I avoid GABA agonists?

Magnesium didn't have a perceptible effect last time I tried it. But my dosage wasn't ~7 grams as you recommended, and it was magnesium citrate, not malate. What about the laxative effects?

The thread to which you linked says Afobazole is GABAergic, but I guess that's different from being a GABA receptor agonist? I also see speculation that it's an MAOI. Even mild MAOIs like Rhodiola rosea tend to keep me awake for a very long time, so that gives me pause.

[ScienceGuy]

I had no idea cannabis effected GABA! On a related tangent, I've read that caffeine is a GABA (as well as adenosine) antagonist. Is it as essential that I avoid GABA antagonists as it is that I avoid GABA agonists?

CAFFEINE inhibits GABA release so ideally would be best avoided; HOWEVER, it is typically NOT advisable to attempt quiting TWO ADDICTIVE SUBSTANCES at THE SAME TIME. Hence, I would suggest you simply limit, but not completely cease your CAFFEINE intake, and do so by switching from drinking COFFEE to limited quantities of GREEN TEA. You will need to note that OTHER CAFFEINE SOURCES include: COCOA, CHOCOLATE, ENERGY DRINKS, DECAFFEINATED COFFEE. You should in particular avoid COCOA and CHOCOLATE since it induces DEPRESSION and EXACERBATES ANXIETY.

Magnesium didn't have a perceptible effect last time I tried it. But my dosage wasn't ~7 grams as you recommended, and it was magnesium citrate, not malate. What about the laxative effects?

MAGNESIUM will not be a 'magic bullet' but WILL most certainly be a highly useful adjunct, especially when taken as the MALATE form and at the up to 6.25 grams (= 1,000mg Mg) total daily dosage.

I would advise spliting the dosage into three, and if you are currently have problems with sleep due to the BENZODIAZEPINE withdrawal then taking a disproportionately higher amount immediately prior to bed will prove helpful in reduced SLEEP ONSET TIME and SLEEP QUALITY. For example, you might like to take 1 gram upon waking, 1 gram in the afternoon and 4.25 grams at bedtime.

The MALATE form of MAGNESIUM is recommended and is distinctly preferred over the CITRATE form; this is due to the following facts:

1) the MALATE will enhance energy production and feeling of wellbeing via enhancement of KREBS CYCLE function. The typical diet is already overlaiden with too much CITRATE and hence MORE CITRATE will if anything only serve to further imbalance the KREBS CYCLE function.

2) The CITRATE form is significantly more LAXATIVE than the MALATE form, which in itself is a reason to avoid it. The dosage regimen that I have recommended for the MAGNESIUM MALATE, namely 1 gram upon waking, 1 gram in the afternoon and 4.25 grams at bedtime, should not cause you to become 'too loose' so to speak; however, in the unlikely event that it does then a simple dosage adjustment will rectify matters.

I would also advise purchase a bulk quantity of EPSOM SALTS (= MAGNESIUM SULPHATE) and add 1 - 2 CUPS to a HOT BATH and soak in it for 10 MINUTES (or more) DAILY such that you will absorb the MAGNESIUM SULPHATE through your skin into your body transdermally. This will have a significant anxiolytic and relaxing effect and combined with the PER ORAL MAGNESIUM MALATE should be highly useful in helping to treat your BENZODIAZEPINE withdrawal symptoms.

The thread to which you linked says Afobazole is GABAergic, but I guess that's different from being a GABA receptor agonist? I also see speculation that it's an MAOI. Even mild MAOIs like Rhodiola rosea tend to keep me awake for a very long time, so that gives me pause.

RHODIOLA ROSEA induces INSOMNIA for a variety of reasons, including the fact that it is a potent ACETYLCHOLINESTERASE INHIBITOR.

I should add that CAFFEINE is in fact a MAO INHIBITOR

AFOBAZOLE does not in fact appear to have ANY direct interaction with the GABA RECEPTORS at all.

AFOBAZOLE’s mechanism of action seems to be that of SIGMA AND MELATONIN RECEPTORS AGONIST and REVERSIBLE MAO-A INHIBITION...

With THERAPEUTIC EFFECTS including: Antidepressant, anxiolytic, and increases BDNF; with good tolerability profile; and no sedation, cognitive impairment or muscle relaxation, etc…

And with demonstrated efficacy in human clinical trials.

SEE THE FOLLOWING:

Neuroreceptor mechanisms of the afobazole effect (2009):
Quote:

The interaction of afobazole (5-ethoxy-2-[2-(morpholino)-ethylthio]benzimidazole dihydrochloride) and its main metabolite M-11 (2-[2-(3-oxomorpholine-4-yl)-ethylthio]-5-ethoxy benzimidazole hydrochloride) with neuroreceptors was studied using the method of radioligand analysis. The binding of afobazole with s1 (Ki =5.9 x 10(-6) M), MTI (Ki =1.6 x 10(-5) M), and MT3 (Ki =9.7 x 10(-7) M) receptors, as well as with a regulatory site of MAO-A (Ki = 3.6 x 10(-6) M) was revealed. The binding of M-11 with MT3 receptors (Ki = 3.9 x 10(-7) M) was demonstrated. The translocation of s1 receptor from endoplasmatic reticulum to the external membrane was revealed by the confocal microscopy technique on the immmortalized hippocampal HT-22 cells under the condition of 30- and 60-min-long afobazole (10(-8) M) application. Afobazole was shown to inhibit MAO-A reversibly. These properties of afobazole are consistent with our previous findings of the anxiolytic and neuroprotective effects of this drug.
^ According to this study AFOBAZOLE interacts with the sigma-1 (s1), melatonin-1 (MT1), and melatonin-2 (MT2) receptors, and acts as a reversible monoamine oxidase A (MAO-A) inhibitor.


Interaction of Afobazole with sigma(1)-Receptors (2009):
Quote:

In vitro radioligand assay revealed interaction of afobazole with sigma(1)-receptors (Ki=5.9x10(-6)M). Translocation of sigma(1)-receptors from the endoplasmic reticulum to the outer membrane was demonstrated by confocal microscopy. Experiments were performed on the model of HT-22 immortalized hippocampal cells after incubation with afobazole in a concentration of 10(-8)M.
^ Reinforces AFOBAZOLE 's sigma-1 activity which appears to be its main mechanism of action.

Afobazole decreases motor side effects induced by haloperidol (2009):
Quote:

Experiments on mice showed that a single intraperitoneal administration of anxiolytic afobazole (10 mg/kg) increases the effect of haloperidol in the apomorphine-induced climbing test and does not influence the catalepsy caused by the neuroleptic agent. The daily dose of afobazole 10 mg/kg during a five-day preliminary test reduced the extrapyramidal effects of haloperidole on rats and mice without significant change of the apomorphine-induced climbing test results. The ability of afobazole to reduce extrapyramidal disturbances caused by haloperidol can be related to the agonist effect of afobazole with respect to sigma 1 receptors.
^ This study shows (or says I mean) that AFOBAZOLE is an agonist at sigma-1.

Antidepressant properties of afobazole in Porsolt and Nomura tests (2009):
Quote:

Anxiolytic afobazole was shown in the experiments on outbred rats to decrease the immobility in the Porsolt and Nomura swim tests. The degree of afobazole effect in a dose of 5 mg/kg (i.p.) is similar to that of the standard antidepressant amitriptyline administered in doses of 10 mg/kg. Data obtained are testifying to the antidepressant activity of afobazole.
^ In addition to its anxiolytic effects, AFOBAZOLE has antidepressant effects comparable to amitriptyline in the rodent Porsolt and Nomura swim tests (whatever those are, I'm assuming they're similar to the forced swim test (FST)).

Selective anxiolytic afobazole increases the content of BDNF and NGF in cultured hippocampal HT-22 line neurons (2009):
Quote:

Experiments on immortalized hippocampal cell culture of mice showed that afobazole increases the NGF level in a final concentration of 10(-8) M and the BDNF level in final concentrations from 10(-8) to 10(-5) M.
Effects of afobazole on the BDNF content in brain structures of inbred mice with different phenotypes of emotional stress reaction (2006):
Quote:

Changes in the BDNF content in brain structures--hippocampus, hypothalamus, striatum, and frontal cortex--were determined in mice of different emotional-stress reaction phenotypes, which were subjected to emotional stress and treated by the selective anxiolytic afobazole. The changes were different in BALB/c and C57BL/6 mice. Afobazole exhibited a significant protector action against a decrease in the brain BDNF level caused by emotional stress in BALB/c mice.
^ AFOBAZOLE increases BDNF expression in the hippocampus and reverses the deficits in BDNF levels induced by stress, further markers of antidepressant efficacy.

Edited by ScienceGuy, 30 January 2012 - 01:05 PM.

[ScienceGuy]

Thanks for the response. You do an excellent job of presenting information clearly and concisely, formatted to be easily readable online.

You're welcome! Thank you for the compliment!

[quamquam91]

One more question: I've been doing some reading and have gotten the impression that benzodiazepines attach to GABA-A. Do I need to avoid all GABA agonists or just GABA-A agonists?

[ScienceGuy]

One more question: I've been doing some reading and have gotten the impression that benzodiazepines attach to GABA-A. Do I need to avoid all GABA agonists or just GABA-A agonists?

Excellent question!

In short, you are quite correct that BENZODIAZEPINES bind to GABA-A RECEPTORS as opposed to GABA-B RECEPTORS; however, down-regulating GABA-B RECEPTORS is something that you wish to AVOID as well; and hence you do indeed want to avoid ALL GABA RECEPTOR AGONISTS.

See this thread in which I comprehensively cover matters and list items which it is OK for you to take and/or which may prove helpful in easing and treating your BENZODIAZEPINE WITHDRAWAL: TREATING ANXIETY SAFELY & EFFECTIVELY

Edited by ScienceGuy, 02 February 2012 - 11:26 AM.

[bkmk]

i feel gabaergic effect from l glutamine 500 mg . at first it incrases anxiety duo to conversion to glutamate then i take some b6 to convert to gaba.for some days i feel sedated . does this way cause gaba receptor downregulation ?

[rogerthat]

Look into Lithium Orotate (low dose)...was and still is the biggest help I've had in a protracted Phenibut withdrawal.

[bkmk]

previous post i said i feel sedated(gaba) from glutamine but i also have periods during the day that i feel to much activated (glutamate ) probably because of glutamine - glutamate -gaba cycle . so dont take l glutamine during benzo withdrawal.

[Introspecta]

Rogerthat Did the Lithium help you to sleep during the Phen withdrawal? I assume it reduced the anxiety. Did it take away the creepy crawly feeling in your skin?

[mycotheologist]

quamquam91: Its been 10 months since a 2 month benzo binge and you still haven't recovered? How has the gotu kola been working out for you? I'm sure you're extremely close to a full recovery. 10 months is an extremely long time for a relatively short duration of use.

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? 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. 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. What about you ScienceGuy, do you have much experience with GABAergic withdrawals or are you speaking purely from theoretical knowledge? Also, I read that kavalactones aren't actually GABA agonists but rather they work by upregulating GABA_a receptors. Brilliant info though, I learned a lot from reading your posts. Do you have any more info on the things that do work?

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. 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.

Edited by mycotheologist, 09 July 2012 - 03:39 PM.

[protoject]

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...

[Rior]

While ScienceGuy has really covered everything very well, I just want to chime in with my own personal experience dealing with benzo withdrawals. Mine weren't so terrible, as I used the benzos themselves to slowly taper myself down, I can surely attest to the value of -Bacopa monnieri- in decreasing one's anxiety and increasing base cognitive functioning. As scienceguy has illustrated, it causes an upregulation of GABA and has been shown to actually *decrease the time* it takes for downregulated GABA levels to return to normal. So, to me, this sounds like it would be exactly what you're looking for.

Although it may be hard news to take in, you must acknowledge that you may have caused real cerebral damage after immediate cessation of use rather than tapering. That said, I would be one to suggest perhaps a cerebrolysin regimen to aid in the recovery of your mental state? While I have yet to try it myself due to a lack of funds, from everything I understand it seems to help people tremendously with issues associated with cerebral damage. That could be a major step in recovering your cognitive ability. Good luck!

[mycotheologist]

Look into Lithium Orotate (low dose)...was and still is the biggest help I've had in a protracted Phenibut withdrawal.

Very interesting, can you elaborate on that a bit? Which symptoms does it help with? What are the side effects? I know that lithium salts are used as mood stabilisers so I'm guessing it prevents anxiety but does it cause anhedonia?