I noticed that there seems to be much more effort (per head of community population) going into researching alternative (not currently in popular useage in the west) entheogens in Australian based communities such as the Coroborree, than there is at eDot or TheNook ( at least until recently). European enthnonbotay sites such as Psychonaut.com have virtually no knew research done by members.
Now there are a number of viable explanations I'm sure.
But here is what I think: Australia had Salvia Divinorum and Kratom made illegal first, and has more restrictions on what can be openly traded. In the US, Salvia is still legal in most states, as is Kratom.
Having Salvia and Kratom legal has caused the US communities to rely on them, and having no reason to research alternatives, they didn't. We on the other hand, have had years of incentive to search for alternatives.
I believe the current increase in interest in alternatives can be mapped against the beginning of the state by state legislation to criminalise Salvia Divinorum, and too a lesser extent Kratom.
Hypothesis: Hostile legislation drives innovative enthnogenic grassroots research.
If his is true, then as Salvia and Kratom (in particular, but not exclusively) are legislated against in more states of the US, more people will put effort into finding alternatives. More people looking equals more potential finds.
A good sociologist should be able test this, especially in retrospective.
It's interesting to note that in countries where salvia and other entheogens are more widely available commercially, this commercial activity does not seem to drive innovation, but often the opposite. If vendors can keep selling Salvia d and Kratom, then why would they bother doing research, other than to find ever stronger extracts. This strikes me as particularly harmful, as the stronger extracts make easier targets (ironically) for hostile legislation.
Therefore I'd further hypothesise that commercialisation of trade in ethnobotanicals can have an adverse effect on their legality. Bt this is a bit more complicated. A better way of putting it might be: Commercialisation of trade in ethnobotanicals can have an adverse effect on their legality, in the absence of research aimed at laterally diversifying the range of species and products available, and a willingness of the vendors to embrace this diversification.
If you chase two rabbits, you will loose them both (Hopi proverb?) The anti-drug/anti-entheogen movement is part of the establishment, and can chase a lot of rabbits at once. In the pat we have given them too few rabbits, now we must endeavour to give them more than even they can chase.
So where does that leave us in term of what to do next. The first step is to avoid despair. A researcher at my uni just finished his PhD on how innovation drives sustainability at a systemic level. Well, if he is right the legislation is forcing us to become more sustainable. Essentially what we nee to do is this: Research, and lots of it. There are bound to be many more plants out there that are useful to us, and even if they are not, our speculations will make good reading for the people watching us, and they might well spend (waste) some time figuring out that we are barking up the wrong tree.
Vendors and customers need to increase the breadth of what they sell and what they buy (respectively). This will make it more difficult for the authorities to pick out an easy target.
Sadly, the hardest thing that we need to do, and this is a lesson that the US community is having a hard time learning, is stop making our activities so media accessible. Without this the previous two suggestions will be less effective, though I believe that they will still work to some extent.
Finally something kind of definitive on Candicine: "Nicotine-like action on the nervous system. In animals it provokes hypertension, while large doses have a curare-like action." Phytochemical Dictionary
USe caution when consuming large amounts of T. spachianius.
N, N, N-trimethyltyramine chloride - Starting to make sense now.
Notes on an argument against criminalisation
What is the philosophical position of the TGA? Are they swayed by rational argument or only raw power? Determining these answers will provide direction in our way forward.
How to combat the position that any drug other than the legal 3 (Alcohol, Tobacco and Pharmaceuticals) should be criminalised? Well that depends on what underlies that position.
"If it's not broken don't fix it" conservatism - respond with 'but it is broken'
"Drugs are dangerous" So are the ones you can buy
"New drugs have unknown potential" - This isn't true as things like saliva are not 'new', so anecdotal data on long term effects is available at least. In any case 'old' drugs esp alcohol have known dangers. How do you weigh an unknown danger vs a known one? It is analytically (in philosophically at least) questionable at best.
"If as many people took new drug A as take old& legal drug B the sky would fall" - respond by calling them out on the basis for this. If everyone smoked SD instead of getting on the piss, then mayhem could ensue, except, if this scenario did come to pass, the situation would be necessarily different to the one we find ourselves in. In any case, what would they base this inference on? Where is the proof? This may be a convenient time to suggest a conspiracy.
"Hallucinogens are inherently bad" - Tricky. Construct parallel arguments showing all intoxicants are inherently bad and then perform reducto ad absurdum. Alternativelty argue that nothing is inherently bad and that any claim that hallucinogens are inherently bad is irrational. Denounces them in the media where you can.
I'm wondering what it is (if anything) that I can do to change the legal status of certain plants, or at least halt the progression of criminalisation of others? can the TGA be lobbied? Can MP's do anything? Would they do anything? Even the Greens have stated that they do not support legalising any drug that is currently illegal.
Should we make the TGA's job as difficult and costly as possible, within the bounds of the law of course - and then complain about the cost to the tax-payer? Maybe. Or not as I think the TGA actually turns a considerable profit.
Should we put all our efforts into finding new plants and novel actives not covered by existing laws/shedules? Almost certainly
Should we take action that attacks the analogue clauses eg: try to get chocolate made illegal as an analogue of 'naughty' PEA's? Not sure.
I worry that an ill-thought-out action could only make matters worse. But I would love to see the TGA drown in red tape, that is for sure.
I know that it takes a lot of people to make a difference, and that we need to be patient, but I want there to be something constructive that we can do now.
Edit: We should all also develop an interest in a career in politics.
Is there an ethical problem with our community relying on animal studies?
Much , if not all, of the data I've dredged up lately has been based on animal testing, not all of it pleasant for the animals concerned. I'm generally against animal testing where it involves causing profound suffering and pain (note, not all animal testing does this) Furthermore animal testing can't really capture the subjective experience of a particular drug as we can't ask the mouse: "What was it like?" I'll leave the obvious "rats& mice aren't humans and therefore have differing metabolisms et" to one side.
So there are two potential problems here.
1. Cruelty
and
2. Lack of usefulness.
To expand on '1' - I don't like cruelty to animals, particularly when there is no good reason for it. So when I find a paper indicating that a certain herb has important analgesic or anti-anxiety effects on mice as ascertained by an experiment that caused the mice pain and suffering, and I use this information to bring to the community's attention an underutilized ethnogen, am I doing something unethical? I'm not sure, but if I am, what do I do about it? What's the ethical position? Do I not utilize studies that use animals in this way, because that rules out most cutting edge research. I don't know and will, think on it some more.
Problem 2 - If we give a rat something, how do we know if it is hallucinating or not, or if it is feeling less anxious, or what the qualitative nature of these feelins are like? I would contend that to a large extent that we don't, and so animal based data can't be a basis for anything other than physiological inferences at best! That these studies could be not so useful, makes the problem of cruelty even worse.
Someone very smart I know summed it up like this in a psych paper she recently wrote: If rats are similar enough to us to provide useful psychological data, then it's unethical to experiment on them. If they are dissimilar enough to experiment on, then they won't provide useful psychological data.
No more obsessively scanning through electronic archives of other peoples work in search of exciting things!
Quit living vicariously and go bioassay something yourself!
"Pharmacological Investigation of Observed Anxiolytic Effects of the Marine Natural Product Aaptamine" Planta Medica 2008; 74
Aaptamine was administered in three doses (5, 10, 15 mg/kg i.m.) and the mice were observed for anxiolytic effects in an established chick social separation-stress model [3]. Results showed that separation-induced distress vocalizations were significantly attenuated in isolated chicks receiving 10 or 15 mg/kg aaptamine (ns = 12; ps < 0.05). However, higher concentrations of aaptamine were reported to induce a transient sedative state followed by motor incoordination. Thus the anxiolytic effects reported at the lower doses may be related to aaptamine's other behavioral effects. In an effort to identify receptor system(s) mediating this behavior, aaptamine was tested for its ability to compete for µ-, δ- and κ-opioid receptor binding (vs. 3H-DAMGO, 3H-DPDPE and 3H–U69593 respectively) in rat brain membranes. The results of receptor binding assays indicated low affinity of aaptamine for all three opioid receptors with Ki values 1.49 ± 0.07 µM for µ- and > 5 µM for δ- and κ-opioid receptors. Other sources cite Aaptamnine as an alpha-adrenergic receptor blocker. Does this explain the effects?
Galphimia glauca - strong depressant activity on the nervous system
http://0-www.thieme-connect.com.library.ne...5/s-2007-981539
"...important anxiolytic effectiveness, very similar to that produced with lorazepam...his compound exhibited an innovative action mechanism and selectively inhibited dopaminergic neurons discharges in the ventral tegmental area [16] without exhibiting interaction with the GABAergic system [17]." Planta Med 2007; 73: 713-717
Cistus creticus - sedative effects
Matricaria recutita (maybe?) - apigenin is central benzodiazepine receptors exerting anxiolytic and slight sedative effects but not being anticonvulsant or myorelaxant.
Cedrol - cedarwood oil Sedative - suggests volatile inahlation
Euphorbia hirta - Analgesic, Antipyretic and Anti-Inflammatory
Egletes viscosa - gastroprotective and peripheral analgesic properties of diterpenes isolated from E. viscosa.
Byrsocarpus coccineus syn. Rourea coccinea - possess a dose determined anxiolytic – sedative activity with no effect on exploratory activity and locomotion.
http://www.ajol.info/viewarticle.php?id=26192
Helichrysums - antibacterial and monoamine oxidase inhibitory activity
http://0-www.thieme-connect.com.library.ne...5/s-2006-949814
Apocynum venetum http://0-www.thieme-connect.com.library.ne.../s-2008-1075172
Planta Med 2008; 74
DOI: 10.1055/s-2008-1075172
Anxiolytic Activity of Apocynum venetum L. and its Proposed Mechanism of Action
O Grundmann1, J Nakajima2, V Butterweck1
1 College of Pharmacy, Department of Pharmaceutics,University of Florida, FL, 32610, USA
2 Tokiwa Phytochemical Co., Chiba 285–0801, Japan
Apocynum venetum (AV, Apocynaceae) is a wild shrub native to parts of northern Asia and the Mediterranean region. A leaf extract from AV has been shown to possess various beneficial effects including antidepressant and anxiolytic activities [1]. This study evaluated further the anxiolytic-like activity of five fractions (A, B, C, D, and E) prepared from an ethanolic AV leaf extract using the elevated plus-maze (EPM) test in mice. Male C57BL/6 mice were either treated orally with AV extract and fractions or diazepam and buspirone as positive control 1 hour before behavioral evaluation in the EPM. A single treatment of AV extract markedly increased the percentage time spent on the open arms of the EPM in doses of 30 mg/kg p.o. and 125 mg/kg p.o., indicating an anxiolytic-like activity. These anxiolytic-like effects were partially antagonized by the benzodiazepine antagonist flumazenil (3 mg/kg i.p.) and the 5-HT1A receptor antagonist WAY-100635 (0.5 mg/kg i.p.). Active fractions of AV according to 30 (fractions C, D, and E) and 125 (fractions A, C, and E) mg/kg of whole extract were also antagonized using flumazenil and WAY-100635. While flumazenil blocked the anxiolytic action of the fractions in a dose equivalent to 125 mg/kg whole extract, WAY-100635 antangonized the fractions according to 30 mg/kg of AV extract. In conclusion, these results indicate that the anxiolytic activity of an AV extract acts via both the GABA (in 125 mg/kg) and serotonin (in 30 mg/kg) receptor systems in a dose dependent manner. References: [1] Grundmann O, et al. (2007)J Ethnopharmacol. 110(3): 406–11.
Salvia cinnabarina http://0-www.thieme-connect.com.library.ne...5/s-2004-818954
A New Diterpenoid with Antispasmodic Activity from Salvia cinnabarina
From the leaf surface exudate of the aerial parts of Salvia cinnabarina a new secoisopimarane diterpenoid with a non-specific spasmolytic activity on histamine-, acetylcholine-, and barium chloride-induced contractions in the isolated guinea-pig ileum was obtained. The IC50 value obtained was comparable with that obtained for papaverine. The structure of 3,4-secoisopimara-4(18),7,15-triene-3-oic acid was established by 1D and 2D NMR spectroscopic techniques.
Egletes viscosa http://0-www.thieme-connect.com.library.ne...5/s-2006-931564
http://rain-tree.com/macela.htm
12-Acetoxyhawtriwaic Acid Lactone, a Diterpene from Egletes viscosa, Attenuates Capsaicin-Induced Ear Edema and Hindpaw Nociception in Mice: Possible Mechanisms
Caroline M. Melo1, Juliana L. Maia1, Ítalo J. M. Cavalcante1, Mary Anne S. Lima2, Gizelle Angela B. Vieira2, Edilberto R. Silveira2, Vietla S. N. Rao1, Flávia A. Santos1
1 Department of Physiology and Pharmacology, Federal University of Ceará, Fortaleza, CE, Brazil
2 Department of Organic and Inorganic Chemistry, Federal University Ceará, Fortaleza, CE, Brazil
Abstract
The diterpene, 12-acetoxyhawtriwaic acid lactone (AHAL, tanabalin) isolated from the flower buds of Egletes viscosa Less. (Asteraceae) was evaluated on capsaicin-induced ear edema and hindpaw nociception in mice. AHAL (12.5, 25 and 50 mg/kg, p. o.) significantly attenuated the ear edema response to topically applied capsaicin (250 μg), in a dose-related manner. At similar doses, AHAL also suppressed the nocifensive paw-licking behavior induced by intraplantar injection of capsaicin (1.6 μg). These responses to capsaicin were also greatly inhibited by ruthenium red (3 mg/kg, s. c.), a non-competitive capsaicin receptor (TRPV1) antagonist. The anti-edema effect of http://www.shaman-australis.com/forum/inde...id=542&st=0
The Corroboree -> Edit entry Yeti101's BlogAHAL (50 mg/kg) seems unrelated to either blockade of mast cell degranulation or to histamine and serotonin receptor antagonism since AHAL did not modify the paw edema response induced by intraplantar injections of compound 48/80, histamine or serotonin. However, the hindpaw edema induced by substance P and vascular permeability increase induced by intraperitoneal acetic acid were significantly suppressed by AHAL. The antinociceptive effect of AHAL (50 mg/kg) was unaffected by naloxone pretreatment but was significantly antagonized by theophylline and glibenclamide, the respective blockers of adenosine and KATP-channels. AHAL (50 mg/kg, p. o.) did not impair the ambulation or motor coordination of mice in open-field and rota-rod tests. These data suggest that AHAL inhibits acute neurogenic inflammation possibly involving capsaicin-sensitive TRPV1-receptors, endogenous adenosine and ATP-sensitive potassium channels.
Perovskia Tetracyclic diterpenes(?) http://0-www.thieme-connect.com.library.ne...5/s-2006-951766
KT botanicals has Perovskia atriplicifolia listed as potentially interesting - roots apparently has similar phytochems as Salvia miltiorrhiza.
Tried out my latest successful Kanna type thing. Equal portions of Sceletium tortuosum (mostly stemmy material), D cooperi (probably) and Aptenia cordifolia (leaves, stems and roots) were fermented in plastic bag in a warm place for about 7 days. After drying in the sun for some time, the process was finished by a quick roast in the oven at 150 C to ensure dryness & to get rid of any remaining oxalates.
Inhaled a lot of the dust that came off when powdering/crushing. Ate a bit of stem (pleaseant nutty/toasty taste). Very strong buzz, much stronger than any sceletium only kanna I made previously. No heavyness in the limbs, quite a pronounced adrenalin like feeling. Pulse didn't rush, but I felt the air was really getting into my lungs.
This is of course not very conclusive by itself as my scelly is very stressed and this could explain the result. I will make preps of each individually over the next few weeks to see what comes out on top.
Haves
Note - I've just moved, so some of this stuff I have less available than usual, and it might take me longer to get my act together than I'd like.
Seeds:
M.G. Heavenly Blue - have plenty of these
Hemia salicifolia (and who doesn't?) Shitloads!
The rest I only have a small amount of each:
Delosperma bosseranum
Salvia splendens
Withania somniferum
L.williamsii
T. spach cuts - about 48cm tip and 40cm (I think) center cuts, some scarring and sunburn.
Other stuff I'll have for trade in spring will (hopefully) include:
Artemnisia verlotiorum plantlets
D.bosseranum plants
Sceletium tortuosum plants/cuttings
Salvia elegans - Pinapple Sage
Salvia involucrata (?)
Erythrina sp seeds and plant material
Plants/cuttings:
Bramhi
Aptenia cordifolia
Wants
Fittonia sp especial albivenis or verschaffeltii
Geogenanthus sp
M.hostilis
Any Cacti!
I was thinking about the ions that migrate towards electrodes in solution. Two thoughts occur to me:
1. Will wiring a plant up with the anode on the aerial parts and the cathode in the soil cause an increased amount of negative ions to migrate out of the soil and into (and up) the plant? (Or the other way around if I have this arse-backwards, I haven't done any physics/electronics for years). If this is the case, then the direction of the current would be an important factor and should produce different results if varied, something that could be put to good use. There should be existing research on this and I'll post links as I find them.
2. If you run current through a solution (aqueous obviously) of an alkaloid salt, will the positive ions, in this case the alkaloid, migrate to the cathode? I think they would. If it forms crystals in its freebase form, then it should literally grow on that electrode! Of course in a dirty solution there would be all sorts of other crud attracted. I don't expect that you can throw a couple of wires into some pedro tea and pull them out with glistening crystals attached a few hours later. But I do wonder if it is worth a try. Surely this is something other people have tried before?
