Tryptameanie

You're not on antidepressants are you? They seriously lower libido and enjoyment, and inhibit orgasm (sexual problems are reported by about three quarters of users, a considerably larger fraction than report improved mood!) This is a problem with most ADs, though SSRIs are generally the worst. It can also be a problem with opiate use- a single dose will usually inhibit orgasm without reducing desire or pleasure (and can enhance sex for many people), but long-term use tends to lead to a pretty severe loss of interest. You might want to try the prescription AD & nicotine-quitting aid bupropion, a mixed dopamine/norepinephrine reuptake inhibitor. It is reported to greatly increase sex-drive (probably via dopamine), and has been used to supplement other ADs to reverse their anti-sexual effects. One of the new serotoninergic ADs with activity at certain 5-HT receptor subtypes as well as at the transporter is also alledged to increase sex-drive. Another possible contributor (to the erection problem rather than the desire one) is vasoconstrictor drugs. These include most stimulants, especially ephedrine, but the big one is nicotine. So, if you smoke a lot and/or take an SSRI, you could try quitting and going on bupropion for a while. Taking tyrosine/phenylalanine may not increase dopamine levels. The rate-limiting step in DA synthesis is catalysed by an enzyme that is saturated (going as fast as it can) at very low tyrosine levels. Increasing tyrosine/phenylalanine in the diet won't cause increased DA synthesis unless your diet is seriously protein deficient. And if you're diet really is that bad, then your problem is likely caused by generalised malnutrition, and you're best bet would be to work on improving it rather than taking specific supplements. The noradrenergic/dopaminergic stimulant properties of Tyr/Phe may be due to formation of various decarboxylated metabolites (amines, eg phenethylamine from direct decarboxylation of phenylalanine), with amphetamine-like catecholamine-releasing properties. Long-term use would then of course cause depleted rather than increased catecholamine reserves. If you want to try DA supplementation, use mucuna seed for it's high l-dopa content (which will increase DA synthesis). I know it's easier said than done, but the best advice is probably to eat better, sleep better, and use less drugs, especially cigarettes. You also need to think about whether the problem is a result of general poor physical or mental health, or whether there is a more specific problem with your sex life (for instance, a relationship that you're not happy with). All the best, Tryp.

Clematis are stunning plants, the flowers are reason enough to grow them whether or not the alledged activity is present. Anyone got any seeds (from any of the genus) to spare? Please PM me and we can arrange a trade.

Excellent :cool: That Bilzor certainly knows his pharmacology- I remember he wrote an interesting series of posts on GABA pharmacology (which is really complex!)a year or so ago, on the "Advanced Drug Discussions" forum at Bluelight.

Ano- ask him for a reference on that and repost the details in a new thread. This should be made widely known, as I imagine many people produce kitchen-chem acetone extracts for personal use and sale.

Benz- the term I've heard used for the effects of the tropane/opiate combo is "twighlight sleep/state", originally used in reference not to recreational consumption, but to use as an pseudo-anaesthetic and amnesic during surgical procedures and childbirth. I understand that in the intended state the patient is semi-conscious, able to respond to the surgeon and to maintain respiration, but is insensitive to pain and unable to form new memories, (hence won't recall the procedure afterwards). The use of this combo carried a much lower risk of death than ether and chloroform. The amnesic effect is useful for repeated procedures that are crucial to the patients life or quality-of-life, but that are so unpleasant that they may be unable to make themselves submit to a second round. Probably the most common situation in modern practice in which tropane amnesia is used is chemotherapy of cancer. Chemo drugs usually produce immediate extreme nausea and vomiting, and need to be administered several times to get a reasonable chance of killing all the tumour cells. Even when the chemo is likely to produce complete remission of an otherwise soon-to-be fatal cancer, and the patient wants to go through with it, the strong aversive conditioning produced can stop them being able to take the tablet or submit to an injection. Scopolamine is anti-emetic and amnesic, so when given before the chemo drug it both reduces the nausea (though not by much) and reduces the strength of the aversion produced. As an aside, patients are often advised not to eat any foods they particularly enjoy prior to the injection, as a strong aversion to the last taste experienced before the onset of nausea occurs in the majority of people, and cannot be overcome by concious, rational thought. For obvious evolutionary adaptive reasons, the connection between a taste and later nausea is particularly strong, easy to acquire and hard to extinguish. A fair proportion are afterwards unable to stand the taste of peppermint, the flavouring in toothpaste. Apoth- could you please indicate the sources which justify the use of morphine in tropane overdose? Many of the major toxic effects are common to both drugs, including reduction/cessation of intestinal motility & of various secretions, respiratory depression, sedation/confusion/delirium/ataxia etc, and coma. What dangerous/harmful effect of tropanes is the morphine meant to reverse? The only explanation I can come up with is that the morphine might induce vomiting Are you sure you don't mean apomorphine (a non-opioid-agonist derivative of morphine used as an emetic)?

Me too! Me too!

Oh, sorry then! What toxic effect(s) does morphine reverse? I'm not sure home-therapy with cholinergics is a good idea. The problems with overshoot hypercholinergic activity are potentially more serious than the original tropane poisoning. I've seen reccomendations that physostigmine not be given as first aid, even by medical professionals in an ambulance, only in a hospital setting. Certainly it should not be a substitute for hospitalisation if life/health is in danger.

I believe Anodyne is researching Kratom for a uni pharmacology paper, hopefully she'll post a reference list (and maybe her finished paper?) as well as any insights she might discover, and I'll also look have a look through the refs and translate the interesting bits from Pharmacese to English for you. [ 27. August 2005, 04:21: Message edited by: Tryptameanie ]

I think prompt hospitalisation is the best idea in cases of serious tropane poisoning, make sure airways are not obstructed and give artificial respiration if needed until an ambulance arrives. If you are very far from hospital, give activated charcoal, and benzodiazepines if seizures develop. At hospital they will probably give cardiovascular support and, in serious cases, physostigmine (a cholinesterase inhibitor which will selectively antagonize the effect). Giving physostigmine outside hospital is not reccomended. I would definitely not reccomend giving opioids or mescaline, which will both likely make things worse (the suggestion above that opium is the "physiological antidote" is wrong and probably derives mainly from the opposite effects on pupil sizes). Remember that tropanes may not be the sole cause cause of unidentified Solanaceae poisoning, and may not be even involved at all, as many other types of toxins including steroids and glycosides are found in the family (eg. as pointed out above, Hajuu was probably at risk of solanine not tropane poisoning, for which the symptoms and treatment are different).

quote: the reason that transgenics is possible is not because organisms share any particular DNA sequences, but because they share the mechanisms for transcription and translation of DNA. And the proteins which carry out these proccesess are coded for where? In the genome. The vast majority of coding genes are shared (at least as close homologues) by the majority of organisms from humans to bacteria. At the biochemical level the common features of organisms vastly outweigh the differences. Arguments about GM need to be based on the ecological and socioeconomic impact of individual applications. More from me later...

Thanks guys, please post anything more as you find it and I'll do the same quote: I'm the least chemically knowledgable person here so it's good you come up with more substantial data and knowledge, in fact its great Umm, don't get me wrong, my theory was really just idle speculation, it just sounded more reasonable to me in light of my knowledge of other drugs than the vague and (apparently) unsubstantiated "spillover" idea. Cheers!

quote: But someone told me that was not at all what I was after, and that Atropa was the only good species of belladonna for human consumption?No, it's full of atropine and thus poisonous. The S. nigrum you found is suitable for human consumption though, apparently making a fairly passable jam quote: I will also care to point out to those who are mortified by the erowid experiences vault on this substance Umm, "mortified" means "extremely embarrassed", which is what you should feel about parading your stupidity for all to see, then ignoring the advice given by knowledgable people who "care" enough about an anonymous fool to try to help them. If you won't listen to the responses, please don't waste space asking questions on these forums.

quote: According to my references, it selectively fills the opiod delta sites first, then when they're all full it overspills to the opiod mu receptors. That's why it has a stimulatory effect at lower doses and a sedative effect at higher doses Do you have a reference from the scientific literature about the "spillover" effect Darklight? The only mention of it I've seen is in Murple's FAQ. The concept is not explained properly and the FAQ was not written by a pharmacogist, but I'm not aware of a mechanism which fits the description given having been described for any other drug (acting at opiate or any other receptors). Without seeing a real reference I'd suspect either poorly informed speculation or a misunderstanding At any rate, the qualitative change in effect with increasing dose could not be explained purely by a change in delta vs mu stimulation. Agonism at both receptor types produces very similiar subjective effects, typical of opioids, (though mu agonists are stronger), so only increasing opioid effects would be expected. I have not seen it confirmed, but a more likely explanation is that the affinity for norepinephrine receptors is higher than for opioid receptors, so a small dose mainly occupies NE receptors. Increasing doses would then linearly increase mu (& delta?) receptor occupany, whereas binding to NE receptors would begin to plateau as full occupancy was approached. This would explain the observed stimulation-sedation transition, though it is likely that differential affinity for, and activity at, the many NE receptors, transporters etc plays some role. Please post any relevant references(not just on "spillover"), I'm very interested in Kratom's pharmacology but the only molecular studies I've been able to find just measured opioid/NE receptor affinities.

quote: But A. muscaria itself seems to agonize choline, yes? Sorta... First, "cholinergic" agonists activate ACETYL-choline receptors, choline is the inactivated form. It used to be thought that the effects of muscaria were due to the muscarine content (muscarine is a selective ACh agonist which gave it's name to the "muscarinic" subtype of acetylcholine receptors. Nicotine is selective for the "nicotinic" subtype). Current opinion is that while muscarine is responsible for some side-effects, (such as sweating and hypersalivation- the opposite to the muscarinic-cholinergic antagonists scopolamine etc), the positive aspects are due to the GABAergic effects of muscimol and ibotenic acid.

I agree with torsten. I'd estimate the relative efficiency of smoking meth(vs IV administration) to be about 40% with the HCl salt and 70-80% with the salt plus bicarb.