mindperformer

Anxiolytics and BZD-active plants

33 posts in this topic

First of all, herbs against anxiety are always a short-time support and not a sole solution. One must work on it, sometimes with sports, sometimes with meditation. Always think "what's the worst that could happen?".

Some anxiolytic herbs (they act on different neurotransmitter-systems):

Paeonia lactiflora- root

Paeonia moutan- root (very active)

Cyperus rotundus- rhizome

Corydalis yanhusuo- root (very active)

Tilia tomentosa (and other Tilia sp.)- flowers

Hypericum perforatum- herb (highly active)

Magnolia officinalis- bark

Passiflora incarnata- leaves (methanol-extracts are highly active)

Salvia miltiorrhiza- root

Valeriana wallichii- root

Evolvulus alsinoides- herb (very active)

Ptychopetalum uncinatum / olacoides- wood

Bacopa monnieri- herb

Rhodiola rosea- root

Erythrina mulungu (highly active)

Eriocephalus africanus- herb

Marsilea minuta- leaves (also has anti-aggressive activity but acts on Serotonin-receptors)

Clerodendrum philippinum syn. C. fragrans- flowers (very active)

Abelmoschus moschatus- seeds

Mumio (Artsch- and Mineral)

Salvia rutilans syn. S. elegans- herb

Chondrodendron tomentosum- bark

Trichosanthes kirilowii- fruit

Albizia julibrissin- leaves, bark and flowers (very active)

Clitoria ternatea- leaves (very active)

Convolvulus pluricaulis syn. C. microphyllus- leaves (very active)

Piper methysticum- root

Sceletium tortuosum- herb

Some plants with compounds, acting on Benzodiazepine-receptors:

Salvia miltiorrhiza- root

Perovskia abrotanoides- leaves (contains Miltirone like Salvia miltiorrhiza)

Salvia canariensis- herb (Galdosol)

Hieracium pilosella- herb

Scutellaria laterifolia- herb

S. barbata- herb

S. baicalensis- herb

Hypericum perforatum- herb

Cyperus rotundus- rhizome

Sesbania grandiflora- flowers

Boerhaavia diffusa- herb (Hypoxanthine also regulates cortisol and because of this a stress-regulator)

Leptospermum scoparium- leaves and honey (Manuka)

Clitoria ternatea- leaves

Tilia tomentosa- flowers

T. platyphyllos- flowers

T. argentea- flowers

Scoparia dulcis- herb

Paeonia lactiflora- root

Paeonia moutan- root

Stachytarpheta cayennensis- leaves

Clerodendrum philippinum- flowers

Hypericum hircinum- herb

Rubus brasiliensis

... with actions on other GABA-subtypes:

Ziziphus spinosa- seeds

Z. jujuba. seeds and fruit

Valeriana officinalis- root

V. mexicana- root

V. celtica- root

V. wallichii- root

Nardostachys jatamansi- root

N. chinensis- root

Sclerocarya birrea ssp. caffra

Cissus quadrangularis- stalks

Angelica sinensis, polymorpha, pubescens- roots

A. dahurica (also acts on GABA-Transaminase)

Ligusticum chinense- root

Comparison of the binding affinity (IC50) on the Benzodiazepine-receptor:

Diazepam… 0,03-0,05 μM (Mindestdosis: 1-2mg)

Flurazepam…0,17 μM

Amentoflavone… 0,006-0,014 μM –Ki: 0,037 μM (main constituent in Dioon edule)

Agathisflavone… Ki: 0,028 μM (Biapigenine) …in Bauhinia vahlii, Rhus pyroides, ...

Xenovulene A… 0,04-0.05 μM (in the fungus Acremonium strictum)

Mayumbine... 0,076 ± 0,0035 μM (in Rauvolfia vomitoria and Corynanthe mayumbensis)

Miltirone…... 0,3 μM (part. agonist. diterpene from Salvia miltiorrhiza; NMDA-R.-Antagonist)

Skullcapflavone (Neubaicaleine)…0,36 μM (auch Ki) (a Flavon from Scutellaria baicalensis)

Phellopterine… 0,4-0,68 μM ~ 0,36 μM (a part. agonist. Furanocumarine from Angelica dahurica)

Hispiduline… 0,8-1 μM –according to other data 1,3 μM

Galdosol… 0,8 μM (a diterpenoide from Salvia officinalis and S. canariensis)

Chrysine (5,7-Dihydroxyflavone)… 2 μM (in Passiflora- species, Diazepam is only 40x as strong)

5,7-dimethoxyflavone… 2,1 μM (in Manuka respectively Leptospermum scoparium)

Wogonine…3-3,6 μM

5-hydroxy-7-methoxy-6-methylflavone... 3,3 μM (in Manuka resp. Leptospermum scop.)

Galangine-3-methylether… 3,5 μM (in galgant- resp. Alpinia galanga- root)

Isoginkgetine… 4-5 μM (a flavone from Ginkgo)

Ginkgetine (Amentoflavone-7,4'-dimethyl ether) … 5 μM (a flavon from Ginkgo)

7-Methoxyrosmanol …7,3 μM

Byakangelicol… 8 μM (a furanocumarine from Angelica dahurica)

Isoquercetine… 10μM

Baicaleine…10,1- 13,1 μM –Ki: 13,1

Imperatorine… 12,3 μM (a part. agonist. furanocumarine from Angelica dahurica and A.sinensis)

Oroxyline… 14,6 μM (also Ki) (in Scutellaria baicalensis)

Cirsiliol…Ki: 20μM at Typ I- BZD- R. (like Zolpidem and displaces Zolpidem)

Tanshinone IIA …20μM (from Salvia miltiorrhiza- root; and also an NMDA-R.-Antagonist)

Scutellarine…21 μM

Apigenine… 30 μMaccording to other data 3 μM (in camomile, parsley and many other herbs)

Carnosolic acid… 33 μM

Luteoline… 49 μM (in Passiflora incarnata, Scoparia dulcis, among others)

Carnosol… 57 μM

α-Casozepin… 88μM (in the casein-fraction of cow-milk)

Kaempferol… 93μM (Ki)

Baicaline…137 μM

Cirsiliol…Ki: 200μM

Acacetine… 3500μM

Obovatol…?

Epinepetalactone…? (Nepeta sibthorpii)

Actinidine…?

Ajmalicine (= Raubasine)…?

6-Methylapigenine…?

Cryptotanshinone…? (from Salvia miltiorrhiza- root; and also NMDA-R.-Antagonist)

Also very promising are the plant-compounds and endogene neurosteroids Allopregnanolone and Epipregnanolone, which act as very strong anxiolytics on GABA-barbiturate-receptors:

Allopregnanolone has strong narcotic, anxiolytic, antidepressive and socialising properties.

The sedative action of allopregnanolone through the barbiturate-GABA-receptor was only observed at low doses. High doses cause the opposite, which can create petulance by inhibiting GABA-receptors. Pregnanolones are much safer than barbiturates.

Allopregnanolone is found in the south-african plant Xysmalobium undulata (uzara- root), which is also used as sedative

The chaste tree (Vitex agnus-castus) contains a Allopregnanolone-precursor: Progesterone in its leaves:

The chaste tree is known as women's herb, but also for men it has healing and potential psychoactive (sedative, anxiolytic) properties. The plant has euphoriant, sedative, anxiolytic, aphrodisiac, antiinflammatory and analgetic actions.

The euphoriant action is mediated through dopaminergic diterpenes (rotundifurane, vitetrifoline, viteagnusine A), which also are responsible for aphrodisiac (hypersexuality) actions through agonistic actions on D2/D3- receptors. There was also found a definitive opioid action on mu-receptors.

The leaves (not the seeds) contain Progesterone, which is the precursor of the endogene neurosteroid Allopregnanolone in our body, which is the endogene neurotransmitter for the barbiturate-GABA-receptor.

The progesterone is active on itself, with anxiolytic actions among others. It is antagonistic on sigma-receptors.

The seeds of the chaste tree indirectly enhance endogene progesterone-levels.

Women use chaste tree- seeds for hormone-regulation.

The iridoids agnuside and aucubine have antiinflammatory, estrogenic and fungicide effects.

Allopregnanolone-amplifier:

Gelsemium sempervirens

16423796-holder-2e7b4d0c3f9ad7ba289ff0212a0ff584.jpg

16423798-holder-8ddd75729353600670f891b2b239e598.jpg

...is really a very dangerous plant, but as always its the dose which decides whether toxic or psychoactive / healing.

This climbing, aromatic plant is used in north- and central-america from indigenous peoples as narcotic. At higher doses it can cause hallucinations.

The main constituents, gelsemine acts pharmacologically contrary to strychnine and possibly could be used as antidote for it, because gelsemine acts also very potent on the glycine-receptors, but activating, while strychnine is a inhibitor on this receptors.

Newer studies reveal an interesting neuropharmacology: The activation of glycine-receptors with very small doses gelsemia-root promote the endogene allopregnanolone- production.

http://www.ncbi.nlm....pubmed/19628662

In my experience already a very small dose has pleasant relaxing and definite anxiolytic action. I used one tenth (1/10) of a tincture from safe 0,05g of the dried root.

BUT: The use (if at all) is only recommended with greatest precaution. It is really a very dangerous plant!

Edited by mindperformer
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The benzodiazepines even were found in humans and plants:

Artemisia dracunculus (tarragon): 100-200 ng/g Delorazepam and 20-30ng/g Temazepam

Solanum tuberosum (potato)- herb: 60-70 ng/g Diazepam, 100-450 ng/g Temazepam and 0,06-0,97 ng/g Oxazepam

Triticum sp. (wheat): 1,6-4,4 ng/g BZDs (N-Desmethyldiazepam, Diazepam, Deschlordiazepam and iso-Diazepam)

human liquor: 1 ng/g Diazepam

human milk: 2 ng/g Diazepam

human serum: 0,001-0,032 ng/g N-Desmethyldiazepam, Diazepam and Oxazepam

To get one small dose delorazepam (0,5mg) one would need to extract 2,5-5kg tarragon-leaves...

To get one small dose temazepam (7,5mg) one would need to extract 16,6kg potato-herb...

Potent extracts of Papaver somniferum (not only opioid) and Nicotiana tabacum also show strong BZD-receptor- binding.

α-Casozepine:

...a tryptic peptide from bovine α(s1)-casein also has benzodiazepine-like activity.

The precursor α(s1)-casein comprises approximately 40% of the casein fraction of cow's milk. Cow's milk also contains morphine, diazepam and opioid-peptides (caso-morphine among others) and has long been considered a tranquilizing beverage with a sleep-inducing and anxiolytic role.

The enzyme trypsin in the gastrointestinal tract hydrolyzes the α(s1)-casein to α-Casozepine, which significantly reduce epileptic symptoms, convulsions and anxiety. It has affinity for the BZD-subunit of the GABA-A- receptor.

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Teotz ?

:unsure:

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i'm not teotz

or do you mean peyote as an anxiolytic?

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Sorry about that.

We had a member here that was a listmaker whose name was Teotz.

Thanks again for another informative post.

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nice one, cheers mp, hours of entertainment in above!

i just want to add specialy for newbies, that one has to always find out if, one can mix any plant herbs with each other.

some herbs, just like medications are contraindicated, and mixing them can cause harm.

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First of all, herbs against anxiety are always a short-time support and not a sole solution. One must work on it, sometimes with sports, sometimes with meditation. Always think "what's the worst that could happen?".

Some anxiolytic herbs (they act on different neurotransmitter-systems):

Paeonia lactiflora- root

Paeonia moutan- root (very active)

Cyperus rotundus- rhizome

Corydalis yanhusuo- root (very active)

Tilia tomentosa (and other Tilia sp.)- flowers

Hypericum perforatum- herb (highly active)

Magnolia officinalis- bark

Passiflora incarnata- leaves (methanol-extracts are highly active)

Salvia miltiorrhiza- root

Valeriana wallichii- root

Evolvulus alsinoides- herb (very active)

Ptychopetalum uncinatum / olacoides- wood

Bacopa monnieri- herb

Rhodiola rosea- root

Erythrina mulungu (highly active)

Eriocephalus africanus- herb

Marsilea minuta- leaves (also has anti-aggressive activity but acts on Serotonin-receptors)

Clerodendrum philippinum syn. C. fragrans- flowers (very active)

Abelmoschus moschatus- seeds

Mumio (Artsch- and Mineral)

Salvia rutilans syn. S. elegans- herb

Chondrodendron tomentosum- bark

Trichosanthes kirilowii- fruit

Albizia julibrissin- leaves, bark and flowers (very active)

Clitoria ternatea- leaves (very active)

Convolvulus pluricaulis syn. C. microphyllus- leaves (very active)

Piper methysticum- root

Sceletium tortuosum- herb

Some plants with compounds, acting on Benzodiazepine-receptors:

Salvia miltiorrhiza- root

Perovskia abrotanoides- leaves (contains Miltirone like Salvia miltiorrhiza)

Salvia canariensis- herb (Galdosol)

Hieracium pilosella- herb

Scutellaria laterifolia- herb

S. barbata- herb

S. baicalensis- herb

Hypericum perforatum- herb

Cyperus rotundus- rhizome

Sesbania grandiflora- flowers

Boerhaavia diffusa- herb (Hypoxanthine also regulates cortisol and because of this a stress-regulator)

Leptospermum scoparium- leaves and honey (Manuka)

Clitoria ternatea- leaves

Tilia tomentosa- flowers

T. platyphyllos- flowers

T. argentea- flowers

Scoparia dulcis- herb

Paeonia lactiflora- root

Paeonia moutan- root

Stachytarpheta cayennensis- leaves

Clerodendrum philippinum- flowers

Hypericum hircinum- herb

Rubus brasiliensis

... with actions on other GABA-subtypes:

Ziziphus spinosa- seeds

Z. jujuba. seeds and fruit

Valeriana officinalis- root

V. mexicana- root

V. celtica- root

V. wallichii- root

Nardostachys jatamansi- root

N. chinensis- root

Sclerocarya birrea ssp. caffra

Cissus quadrangularis- stalks

Angelica sinensis, polymorpha, pubescens- roots

A. dahurica (also acts on GABA-Transaminase)

Ligusticum chinense- root

Comparison of the binding affinity (IC50) on the Benzodiazepine-receptor:

Diazepam… 0,03-0,05 μM (Mindestdosis: 1-2mg)

Flurazepam…0,17 μM

Amentoflavone… 0,006-0,014 μM –Ki: 0,037 μM (main constituent in Dioon edule)

Agathisflavone… Ki: 0,028 μM (Biapigenine) …in Bauhinia vahlii, Rhus pyroides, ...

Xenovulene A… 0,04-0.05 μM (in the fungus Acremonium strictum)

Mayumbine... 0,076 ± 0,0035 μM (in Rauvolfia vomitoria and Corynanthe mayumbensis)

Miltirone…... 0,3 μM (part. agonist. diterpene from Salvia miltiorrhiza; NMDA-R.-Antagonist)

Skullcapflavone (Neubaicaleine)…0,36 μM (auch Ki) (a Flavon from Scutellaria baicalensis)

Phellopterine… 0,4-0,68 μM ~ 0,36 μM (a part. agonist. Furanocumarine from Angelica dahurica)

Hispiduline… 0,8-1 μM –according to other data 1,3 μM

Galdosol… 0,8 μM (a diterpenoide from Salvia officinalis and S. canariensis)

Chrysine (5,7-Dihydroxyflavone)… 2 μM (in Passiflora- species, Diazepam is only 40x as strong)

5,7-dimethoxyflavone… 2,1 μM (in Manuka respectively Leptospermum scoparium)

Wogonine…3-3,6 μM

5-hydroxy-7-methoxy-6-methylflavone... 3,3 μM (in Manuka resp. Leptospermum scop.)

Galangine-3-methylether… 3,5 μM (in galgant- resp. Alpinia galanga- root)

Isoginkgetine… 4-5 μM (a flavone from Ginkgo)

Ginkgetine (Amentoflavone-7,4'-dimethyl ether) … 5 μM (a flavon from Ginkgo)

7-Methoxyrosmanol …7,3 μM

Byakangelicol… 8 μM (a furanocumarine from Angelica dahurica)

Isoquercetine… 10μM

Baicaleine…10,1- 13,1 μM –Ki: 13,1

Imperatorine… 12,3 μM (a part. agonist. furanocumarine from Angelica dahurica and A.sinensis)

Oroxyline… 14,6 μM (also Ki) (in Scutellaria baicalensis)

Cirsiliol…Ki: 20μM at Typ I- BZD- R. (like Zolpidem and displaces Zolpidem)

Tanshinone IIA …20μM (from Salvia miltiorrhiza- root; and also an NMDA-R.-Antagonist)

Scutellarine…21 μM

Apigenine… 30 μMaccording to other data 3 μM (in camomile, parsley and many other herbs)

Carnosolic acid… 33 μM

Luteoline… 49 μM (in Passiflora incarnata, Scoparia dulcis, among others)

Carnosol… 57 μM

α-Casozepin… 88μM (in the casein-fraction of cow-milk)

Kaempferol… 93μM (Ki)

Baicaline…137 μM

Cirsiliol…Ki: 200μM

Acacetine… 3500μM

Obovatol…?

Epinepetalactone…? (Nepeta sibthorpii)

Actinidine…?

Ajmalicine (= Raubasine)…?

6-Methylapigenine…?

Cryptotanshinone…? (from Salvia miltiorrhiza- root; and also NMDA-R.-Antagonist)

Also very promising are the plant-compounds and endogene neurosteroids Allopregnanolone and Epipregnanolone, which act as very strong anxiolytics on GABA-barbiturate-receptors:

Allopregnanolone has strong narcotic, anxiolytic, antidepressive and socialising properties.

The sedative action of allopregnanolone through the barbiturate-GABA-receptor was only observed at low doses. High doses cause the opposite, which can create petulance by inhibiting GABA-receptors. Pregnanolones are much safer than barbiturates.

Allopregnanolone is found in the south-african plant Xysmalobium undulata (uzara- root), which is also used as sedative

The chaste tree (Vitex agnus-castus) contains a Allopregnanolone-precursor: Progesterone in its leaves:

The chaste tree is known as women's herb, but also for men it has healing and potential psychoactive (sedative, anxiolytic) properties. The plant has euphoriant, sedative, anxiolytic, aphrodisiac, antiinflammatory and analgetic actions.

The euphoriant action is mediated through dopaminergic diterpenes (rotundifurane, vitetrifoline, viteagnusine A), which also are responsible for aphrodisiac (hypersexuality) actions through agonistic actions on D2/D3- receptors. There was also found a definitive opioid action on mu-receptors.

The leaves (not the seeds) contain Progesterone, which is the precursor of the endogene neurosteroid Allopregnanolone in our body, which is the endogene neurotransmitter for the barbiturate-GABA-receptor.

The progesterone is active on itself, with anxiolytic actions among others. It is antagonistic on sigma-receptors.

The seeds of the chaste tree indirectly enhance endogene progesterone-levels.

Women use chaste tree- seeds for hormone-regulation.

The iridoids agnuside and aucubine have antiinflammatory, estrogenic and fungicide effects.

Allopregnanolone-amplifier:

Gelsemium sempervirens

16423796-holder-2e7b4d0c3f9ad7ba289ff0212a0ff584.jpg

16423798-holder-8ddd75729353600670f891b2b239e598.jpg

...is really a very dangerous plant, but as always its the dose which decides whether toxic or psychoactive / healing.

This climbing, aromatic plant is used in north- and central-america from indigenous peoples as narcotic. At higher doses it can cause hallucinations.

The main constituents, gelsemine acts pharmacologically contrary to strychnine and possibly could be used as antidote for it, because gelsemine acts also very potent on the glycine-receptors, but activating, while strychnine is a inhibitor on this receptors.

Newer studies reveal an interesting neuropharmacology: The activation of glycine-receptors with very small doses gelsemia-root promote the endogene allopregnanolone- production.

http://www.ncbi.nlm....pubmed/19628662

In my experience already a very small dose has pleasant relaxing and definite anxiolytic action. I used one tenth (1/10) of a tincture from safe 0,05g of the dried root.

BUT: The use (if at all) is only recommended with greatest precaution. It is really a very dangerous plant!

The benzodiazepines even were found in humans and plants:

Artemisia dracunculus (tarragon): 100-200 ng/g Delorazepam and 20-30ng/g Temazepam

Solanum tuberosum (potato)- herb: 60-70 ng/g Diazepam, 100-450 ng/g Temazepam and 0,06-0,97 ng/g Oxazepam

Triticum sp. (wheat): 1,6-4,4 ng/g BZDs (N-Desmethyldiazepam, Diazepam, Deschlordiazepam and iso-Diazepam)

human liquor: 1 ng/g Diazepam

human milk: 2 ng/g Diazepam

human serum: 0,001-0,032 ng/g N-Desmethyldiazepam, Diazepam and Oxazepam

To get one small dose delorazepam (0,5mg) one would need to extract 2,5-5kg tarragon-leaves...

To get one small dose temazepam (7,5mg) one would need to extract 16,6kg potato-herb...

Potent extracts of Papaver somniferum (not only opioid) and Nicotiana tabacum also show strong BZD-receptor- binding.

α-Casozepine:

...a tryptic peptide from bovine α(s1)-casein also has benzodiazepine-like activity.

The precursor α(s1)-casein comprises approximately 40% of the casein fraction of cow's milk. Cow's milk also contains morphine, diazepam and opioid-peptides (caso-morphine among others) and has long been considered a tranquilizing beverage with a sleep-inducing and anxiolytic role.

The enzyme trypsin in the gastrointestinal tract hydrolyzes the α(s1)-casein to α-Casozepine, which significantly reduce epileptic symptoms, convulsions and anxiety. It has affinity for the BZD-subunit of the GABA-A- receptor.

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Combinations can be problematic with high doses of Kava and St. John's Wort, because they are strongly interacting with CYP 450- enzymes in the liver:

http://www.unifra.br/pos/aafarm/downloads/_interaction%20kava%20and%20st_%20johns%20wort%20with%20drugs.pdf

Personally I experienced discomfort and high spirits with a combination of standard-doses of Rhodiola + Hypericum + Passiflora

The St. John's Wort (Hypericum) and Kanna (Sceletium tortuosum) are potent monoamine- enhancers in the brain and as such potentially dangerous in combinations.

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Your plant knowledge is amazing. You should make a wiki / blog..

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Nice list :)

I've had some big problems with anxiety in the past...and continue to do so, although I mostly manage it better these days. For the most part all my experimentation with herbs as sedatives and anxiolytics was fruitless (to me at least). I did have one nice, smooth experience with passionflower tea (could have been placebo), but I usually need a relatively high dose of benzodiazepines to calm me down properly...so from time to time if things get rough I'll get my doc to write me a script.

I've been meaning to try beta blockers as a non-addictive alternative, but haven't gotten around to it yet.

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did you try a psychotherapy? it sounds pathological to me, so benzos and the plant-equivalents are no solution, only sporadic at very severe emerges.

within a psychotherapy Boerhaavia diffusa with a strong Passiflora-extract can be helpful.

Rhodiola and Withania can help too.

Edited by mindperformer

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did you try a psychotherapy? it sounds pathological to me, so benzos and the plant-equivalents are no solution, only sporadic at very severe emerges.

within a psychotherapy Boerhaavia diffusa with a strong Passiflora-extract can be helpful.

Rhodiola and Withania can help too.

mp, australia has a social health care system, but it's not like austria. psychotherapy is out of reach for all but the very wealthy australians.

you might be able to see a shrink if you are in a closed system or suffer from acute psychosis, but that's that.

no therapies available for any of us, 30min with a psychiatrist will cost you 120aud, a sure way to keep your anxieties, because of lack of goverment help.

if you live in the countryside, you often can't see even a doctor or a dentist, that's why everybody drinks a lot of booze, it helps with the anxiety and the toothache!

st. johns wort, my body doesn't agree with, it gave me wiered side effects, inside my head, once i stopped taking it, the symptoms went away, and never returned.

Edited by planthelper

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Thats a load of crap incorrect^

Medicare will cover 1 free sesion with a psychiatrist & 6 free sessions with a psychologist if reffered to by a doctor & six more sessions if the doctor gives another referal or will give you a rebate for the same if you qualify & if you don't well you are earning more than enough to pay for it.

I have found the countryside to be far better than small cities for docs & dentists, easier to get into & better quality but then again they are payed more & do'nt even get me started on city emergeny room wait compared to country...

Edited by ballzac
Please phrase things in a civil manner

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^^ yes and no. You can get a "mental health treatment plan" from a GP, which covers those sessions you mentioned...but it's generally only with very mainstream (and not often very helpful, IME) psychologists who accept bulk-billing...I could be wrong though. I've never had much luck with the CBT approach, and most psych's I've seen I felt were full of crap...I have been meaning to try EMDR therapy for a while but I won't have the time or money for quite some time.

@mp: yeah, the benzos (or any medication really) are more of a band-aid over the bigger problem really...but like PH says, it can be difficult to get good treatment if you're not able to fork out for it. At the end of the day though, there's a chance that my problems may not even be treatable psychologically...and I don't like dwelling on it or feeling sorry for myself - I'd rather just do what I can and get on with the business of life :)

Edited by gtarman

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My experience with psychotherapy in 2009/10, was that I had a doctors prescription and a good chunk of the charge was covered by medicare. The bill was around $60 for a 1 hour a session with rebate. He offered me free sessions of 30 minutes but I only took one because I personally didn't find it as effective.

I found that psychotherapy in combination with an anti-depressant over the course of two or three months was quite helpful at the time.

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Yeah like I said you can get the rebate if you do'nt want a bulk biller. Pretty sure you can get anothter 1 or 2 psychiatrist sessions & even another 6 psychologist sessions if the doc gives you a referral.

Wether it personaly helps you or not is a whole other thing.

Edited by shruman

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Yeah like I said you can get the rebate if you do'nt want a bulk biller. Pretty sure you can get anothter 1 or 2 psychiatrist sessions & even another 6 psychologist sessions if the doc gives you a referral.

Wether it personaly helps you or not is a whole other thing.

rebate, oh yes, but it's still too expensive for any kind of treatment.

and if you get a referal to see a shrink 7 times, they only give you an appointment via the accute team. if the accute team say's you are not psychotic they will not see you.

Edited by ballzac
Ad hominem attack

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"Standard allowable sessions capped at 10 from 1 November 2011

The number of sessions of psychological treatment a client could receive in a calendar year was cut from a maximum of 18 sessions in ‘exceptional circumstances’ to a maximum of 10 sessions, effective from 1 November 2011. The cap of 10 allowable sessions per calendar year also applies to group sessions delivered under the Better Access initiative.

Reinstatement of ‘exceptional circumstances’ sessions from 1 March 2012 until 31 December 2012

Early in 2012 the Government announced interim arrangements to reinstate the ‘exceptional circumstances’ sessions to enable a period of adaptation. The interim arrangements only apply for a transitional period from 1 March 2012 to 31 December 2012.

The maximum standard number of rebatable sessions per calendar year under the Better Access initiative remains at 10 sessions. However, during the transitional period, eligible clients where ‘exceptional circumstances’ apply can receive up to an additional six sessions to bring the maximum total number of allowable sessions in 2012 to 16 sessions.

An information sheet outlining the transitional arrangements for accessing the additional sessions under exceptional circumstances can be downloaded below. Members are particularly alerted to information on the eligibility and documentation requirements for the exceptional circumstances sessions. Included in the information sheet is clarification of Better Access referral and reporting requirements under various circumstances, based on recent advice received from the Australian Government Department of Health and Ageing."

http://www.psycholog...ss/changes2012/

Yeah it was 18 free sessions but then got canned to 10 then extended back to an aditional 6 for exceptional circumstances.

"shruhman don't talk to me on the forum, you cause me enormous anxiety."

You have the luxury of putting me on ignore but as you are a mod I do not no matter how many times I have asked for it...

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in Austria the situation isn't much better, although Sigmund Freud was born here. You only get 20€/ month from health insurance for psychotherapy, which i think is the most constructive, depending on the therapist. Psychologists and psychiatrists should be payed completely by health insurancee.

Edited by mindperformer

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Shruman, if you think mental care is easy available do so.

it is not, according to my experiences (and i had the form which ought to make you see a shrink or psychologist 7 times), and it didn't work.

Edited by ballzac
some comments were irrelevant due to the referred to posts being removed

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I don't want to sound insensitive to the latter comments in this thread but could people please leave the arguments to another discussion?

I'm happy to split this thread to leave room in chill space for the discussion about the efficacy, or lack thereof, of Australia's 'mental health system' but it's unfair to drain such a well composed initial post by mindperformer with such details.

If you'd like this discussion to continue, let me know and that will be done elsewhere.

Best wishes to all.

While I'm at it:

Excellent compilation, mindperformer.

One thing to be careful of, by those using the lists, is confusing affinity with anxiolytic activity.

For example:

"Amentoflavone… 0,006-0,014 μM –Ki: 0,037 μM (main constituent in Dioon edule)"

While showing a relatively impressive affinity, it is a negative modulator of the GABAA receptor at the benzodiazepine binding site and may actually be anxiogenic, if it’s active at all [see article].

There are many variables that might render even seemingly effective compounds inactive as anxiolytics in vivo in humans

There are a couple of good review articles that are worth a read:

Modulation of Ionotropic GABA Receptors by Natural Products of Plant Origin

Flavonoid modulation of GABAA receptors

Flavonoids as GABAA receptor ligands: the whole story?

Flavonoids and the CNS

I might continue adding to this list but for starters:

Rhusflavone from Rhus parviflora; postive GABAA modulator at BZD site (0.045 μM), potent sedative-hypnotic (rodent) [ref].

From Magnolia officinalis:

4-O-methylhonokiol - potent GABAA modulator, orally active (rodent) [ref]

Honokiol - GABAA modulator at BZD site and other GABAergic activity, oral administration in rodents shows potent anxiolytic activity after 7 days administration (greater potency than diazepam) [1, 2, 3]

Magnolol - GABAA modulator at BZD site, active as an anxiolytic/sedative in rodents [ref]

Anxiolytics of comparable efficacy to lorazepam in humans:

Oral lavender oil

Galphimia glauca (galphimine-B )

Edited by Alchemica
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you are absolutely right, and because of this I didn't took the affinities as alone determining the anxiolytic potential.

There are many GABA-receptor- subtypes and as you wrote there are full agonists, partial agonists, competitive antagonists and so on...

I agree with the anxiolytic activity of the Magnolia officinalis -constituents, lavender and galphimia. Magnolia-bark works for me as a good sedative too. Lavender acts also aromatherapeutical.

A little insight in the complexity of GABA- Glycine- and GHB-receptors:

GABA- receptors: GABAA, GABAB, GABAC

endogene ligands: Diazepam, N-Desmethyldiazepam, GABA, (Glycine),

β-CCP (β-carboline-3-carboxylat) (inverse agonist),

Oxazepam, Tribuline BZc und BZp, Hemine und

Protoporphyrine IX, Inosine, Hypoxanthine

Endozepines: Diazepam-binding-Inhibitor (DBI),

human endozepine (hEP), Triakontatetra-

neuropeptide (TTN), Octadeca-neuroepetide

(ODN),

Neurosteroides: PREG (Pregnenolone)- Sulfate, Androsterone,

DHEA (Dehydroepiandrosteron)- Sulfate,

3 alpha-5 alpha-THPROG (Allopregnanolone),

Epipregnanolone, und THDOC (Tetrahydrodeoxy-

corticosterone),

Psychoactive used substances: Agonists: Muscimol, Ethanol, N2O,

Valeranon, Withania somnifera-

constituents, Borneol (partially),

Coreximine, Acorus gramineus-

H2O-Extr., Diethylether,

Clomethiazol, Gelispirolide,

Riligustilide, Ligustilide,

Safranal, Paeoniflorine,

Gaboxadol,

positive allosteric modulators: 6-Methylflavone, Androsterone,

Borneol, Etomidat, Thymol,

Allopregnanolone, Propofol,

Antagonists: α-Thujone,

Arecaidine, Tabernanthine,

Gelsemine, Bicuculline,

Thymoquinone, Piracetam (?),

water fraction from

Acorus gramineus,

Inverse agonists: b-Carboline,

modulators/activators: Protopine, Scoulerine,

Corydaline, Cryptopine,

Tetrahydropalmatine,

Allocryptopine, Withania

somnifera- extr., Scoparinol

(potentiates Barbiturates),

Kalanchoe pinnata- constituents

(potentiates Barbiturate),

Amentoflavone (negative

modulators), Isocurcumenol,

Magnolol & Honokiol

(additive pos. modulators),

α-Pinen,

Selective on α[1]β[2]γ[2L]- subunit: Agonists:

Antagonists: Bilobalide,

Action on Chloride-Ionchannel: Agonists: Etifoxine, Carnosol,

Carnosic acid,

Antagonists: Picrotoxine,

Selekt. ß2 or ß3- subunits: inverse agonists: Loreclezol,

Ethyl-β-carbolin-3-carboxylate (β-CCE),

Methyl-β-carbolin-3-carboxylate (β-CCM),

Valerenic acid, Etomidate,

Benzodiazepine-subunit:

While ligands with high affinity for the α1-subunit rather cause sedation, the α5-subunit is responsible for ataxia and amnesia. Ligands with high affinity for α2- und α3- subtypes generally have higher anxiolytic activity. Anticonvulsive effects are triggered by all subtypes, but mainly by α2-selective agonists. Necessary for a "classical" benzodiazepine- effect (such as Diazepam) is additionally the γ-subunit of the receptor.

The muscle relaxant and anxiolytic action is also responsible for euphoria and addiction potential. Zolpidem has a higher selectivity than diazepam for the α1-subtype. Flavonoids (also Amentoflavone) act weaker on the (among other) α1ß2γ2-subtype. Receptors with α1ß2γ2 are inhibited by a high dose of Apigenin, while a low dose potentiated the binding of Diazepam.

However, hispidulin is a relatively unselective positive allosteric modulator of α1,2,3,5,6ß2γ2-subtypes, but mainly on α1,2,5ß2γ2.

Oxoxylin A from Scutellaria baicalensis is a neutralizing allosteric modulator and is inhibiting the anxiolytic, muscle relaxing, but not the sedative action of diazepam.

6-Hydroxyflavone prefers α2- and α3- over α1- and α5- subtypes and thus has only anxiolytic effects.

Flunitrazepam causes (yet after two days intake) a down-regulation of the α1-subunit. It is potentiating GABA on α1-,β2-,γ2-receptors and decreasing its action on α6-,β2-,γ2-receptors.

Besides it is a α2-adrenoceptor-agonist.

Agonists: Diazepam (acts mainly on

α1-γ2- and also α2,α3,α5-γ2 -

subtypes)

and other Benzodiazepines like

Temazepam in tarragon,

(Kawain, Dihydro-Methysticine,

Yangonin ?), 6-Methylapigenin,

Tanshinone, Scutellarin,

Chrysin, Flavone, Apigenin,

Wogonin, Hispidulin,

Melatonin bei hoher Dosis,

Miltiron, Ajmalicin (=

Raubasin), Galdosol,

Linarin, Ethanol, Diethylether,

Methaqualon, Baicalein,

Baicalin, 7-Methoxyrosmanol,

Skullcapflavon I u. II,

Kessyl-glycol-diacetat (Baldrian),

Hesperidin, Hesperetin,

Amentoflavon, Phellopterin,

dl-Tetrahydropalmatin (?),

Akangelicol, Imperatorin,

Cirsiliol, Carnosol, Paeonol,

Carnosolsäure, Oroxylin,

Oryzagenin, Ginkgetin,

Isoginkgetin, Agathisflavone,

Hydroxypinoresinol,

Kaempferol, α-Pinen,

Inosin (Cordyceps sin.),

Hypoxanthin, Xenovulen A,

Mayumbin,

partial agonists: Imidazenil, Bretazenil

Antagonists: Flumazenil, Harman,

Piracetam (?), Taurin,

6-Methylflavone,

Inverse agonists: R015-4513, Tabernanthin,

Harmine, Harmaline, Harman,

Harmalol,

BZD- potentiators: 4-Hydroxybenzaldehyd (in

Gastrodia elata),

4-hydroxy-3-methoxy=

benzaldehyd (Vanillin),

selective on ω1-BZD-subunit: Agonists: Zolpidem, Alpidem, Zaleplon,

>only sleep induction TZP, Cirsiliol, Quazepam

selective on omega2- and espec. omega3- subunit: Agonists: Zopiclone, Suriclone, Pagoclone,

Antagonisten: β-CCT,

selective on α5- subunit: Agonists: QH-II-66 (a Benzodiazepine- derivatve),

(−)-Epigallocatechin gallat, Ethanol,

Inverse Agonists: β-CCM, β-CCE, L-655,708,

selective on α3- subunit: Agonists: Adipiplon,

selective on ω2-BZD-subunit: Agonists: Clobazam, Arfendazam,

Lofendazam,

Barbiturate-subunit:

With low doses barbiturates: positive allosteric modulation of the GABA-receptor (like the Benzodiazepines).

With higher doses barbiturates: direct activation of the chloride channel of the receptor.

The modulation at lower doses will lead to longer CL-channel-openings in presence of GABA (Benzodiazepines cause more frequent channel openings).

Agonists: Pentobarbital, Phenobarbital,

Secobarbital ua. Barbiturate,

(Allo)- und (Epi)-Pregnanolon

(endogen), 5α-tetrahydro=

deoxycorticosteron (α-THDOC)

(endogen), Etazolat, Tricazolat,

Clomethiazol,

Antagonists: Bemegrid, Picrotoxinin,

ZyclicPhosphate,

Coriamyrtin,

GABA-B-receptors: Agonists: Baclofen, GHB, Phenibut

Antagonists: Passiflora-Benzoflavones,

GABAA-rho -Rezeptor ?

Mitochondrial Benzodiazepine- Receptor: MBR, PBR od. MDR

or „Diazepam Binding Inhibitor- Receptor“ or BZRP (Benzodiazepine receptor peripheral),

Endogene ligands: Porphyrine (mainly Hemin und Protoporphyrin IX,

Diazepam, Desmethyldiazepam, DBI (Diazepam

Binding Inhibitor), DBI-(17-50), Endozepine,

Psychoactive used substances: Agonists: 2-Phenylindol-3-acetamides

like Zopiclon, Alpidem,

Zolpidem among others, Clonazepam,

THDOC (Neurosteroid),

4'-chlorodiazepam,

AC-5216, ALX-620-045,

Diazepam, Flunitrazepam

(the last: less selective),

Antagonists: PK11195,

GABA-Reuptake-Transporters:GAT-1, GAT-2, GAT-3, BGT-1

Endogene ligands: GABA, Na+- Ionen

Psychoactive used substances: Inhibitors: CI966, NO711, ®-Tiagabin,

3-(Aminomethyl)-2,6-difluorphenol,

R(+)-4-methylaminocrotonic acid,

Nipecotic acid, Arecaidin,

Guvacin, Cannabidiol, Δ9-THC,

ß-Alanin, Hyperforin,

GABA-Transaminase: UGA1 (enzyme which degrades GABA)

Endogene ligands: GABA

Psychoactive used substances: Inhibitors: Valproic acid, Imperatorin,

Falcarindiol, Gastrodin,

4-Hydroxybenzaldehyd,

4-hydroxy-3-methoxy=

benzaldehyde (Vanillin),

Glutamate-decarboxylase: GAD (enzyme which degrades GABA):

Endogene ligands: GABA, Vitamin B6 (pyridoxal phosphat) as Cofactor

Psychoaktive used substances: Activators: ®-3-methyl-GABA,

Inhibitors: Allylglycine,

Glycine- receptors: GlyR

Endogene ligands: Glycine, L-Serin, Taurin, Hypotaurin, L-, D- und β-Alanin

Psychoaktive used substances: Agonists: Strychnine, Brucin, Taurin

Antagonists: 2-amino-5-bromo-2'-chlorobenzophenon

(ABPH)- ein Phenazepam- Metabolit,

Gelsemine,

Glycine-transporter: GlyT1, GlyT2

Endogene ligands: Glycin

Psychoaktive used substances: Activators:

Inhibitors: ALX 5407, Sarcosin

GHB- receptors: GHB-R

Endogene ligands: GHB, Trans-4-Hydroxycrotonic acid

Psychoaktive used substances: Agonists: Na-GHB, K-GHB, t-HCA,

4-Hydroxyvalerate,

Antagonists: NCS-382

Upregulators: Sulpirid, Amisulprid

Edited by mindperformer

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The anxiolytic promising 6-Hydroxyflavone is the main constituent of Barleria prionitis.

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Be aware of deducing psychoactive effects only from neurological findings of a plant with unknown psychological action. The neurological interrelationships are extremely complex and there are always new findings. They can only be used as a hint.

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More on Ziziphus spinosa seeds:

I think they are the most promising herb for long-term- therapy against anxiety, especially mixed with Magnolia bark (traditionally combination in China).

The most exciting found was that Sanjoinine A, an anxiolytic cyclopeptide alkaloid in it, increased the quantity of GABA-benzodiazepine-type receptors themselves (by increasing gamma-subunit expression) AND increased GABA synthesis via GAD65/67 activation, so it enhanced the expression of glutamic acid decarboxylase, an enzyme that catalyzes the decarboxylation of glutamate to GABA.

This causes a sustainable effect by increased BZD-receptor- quantity and increased GABA- production.

Except from the Sanjoinine, Z. spinosa-seeds contain Jujuboside A1, C and Acetyljujuboside B, which are inhibitors of histamine release and Nuciferine (also in blue lotus and a dopamine receptor inhibitor). Jujuboside A also inhibits glutamate-induced calcium enhancement. Swertisin (a flavonoid) was also found to have a modulating effect on the GABA-system and the flavonoid Spinosin had an sedative effect. The D-Coclaurine blocks postsynaptic D-receptors.

The leaves contain the sweetness-blocker Ziziphin.

The seeds act as an anxiolytic in low doses and as a sedative in higher doses, and also show an effectiveness in reducing pain sensation and increasing pain tolerance. It was also tested against narcotics withdrawal symptoms and alcohol withdrawal.

It was found, that roasting (traditional in China) makes them more active because the Sanjoinine A is heat-converted to the more active Sanjoinin Ah1.

I use 3-10g (up to 20g) of the grinded seeds for a single dose. It is also possible to make a tincture.

By the way: Scutellaria baicalensis contains not only the anxiolytic flavonoids but also a high amount of the famous endogen sleep hormone Melatonin:

http://www.herbs.org/current/melatonin.html

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