yeah i will be continuing my reports. definitely feel that 4mg was about right for me, or about 0.0533mg/kg. the longer i'm awake without sleep the more pleasant the prospect of sleep sounds.
the 'which way is poland' headspace appears to be typical first dose response to this material, after that it gets more self conscious and uncertain. also i'm not sure about the halflife thing, everyone's brain has different metabolic capacities and tolerance buildup rates and so forth. i am fairly certain i was drifting off or definitely asleep when my alarm went off at 3am this morning because it startled me, so the 4mg was letting me sleep at t+12hrs.
the beneficial effects on my ADD are still present however. i did my hour ride today and i've vacuumed my flat and done a bunch of research and stuff. i'm tired tho, sleep will be very much welcome to me tonight. i had a small booster at about 10:30am of maybe 2mg and to be honest the extra stimulation is not pleasant but not unpleasant either. i had a little euphoria in the first 6 hours or so but i think that was also in part due to normal feeling good after eating and being pleased about the arrival of something that seems so far to be a possible effective treatment that i can actually access and won't have any trouble keeping under contrtol.
my only concern is, precisely what you are talking about - whether it disrupts my sleep. and if this proves to be problematic i am wondering what tactics could be applied to ameliorating this, having the weekend off, for example, increased water intake, antioxidants, and so forth. i hear nonsense - well, non-scientific claims that things like oranges cause the more rapid wearing off with methamphetamine... knowing what its metabolites are may help, and there has been at least one report in this thread of polyphasic activity suggestive of at least primary active metabolites (and possible avenues of SAR exploration).
anyway, since i was drawn away from this post writing mid-thread by something or other, i've had a bit more time in between to think about things and observe my response and i have noticed that it causes me to have a really quite strong anxiety reaction, more in the paranoia realm of anxiety, so i am trying raising my dose of mebicar to see if this addresses it, as this anxiety is less generalised than what i got from mdpv, and the CNS stimulation is definitely much stronger so i should not find near as much sedating effect (which is an odd reaction to mebicar anyway), and this brings my dose rate for mebicar up to more like 600-750mg/day.
i will continue to report my responses and doses and times and reflections for a little longer at least, when i first read this i was hoping that someone else who has a similar condition to me tried it but not as much as i would have liked (actually nobody else other than speculatively).
edit:
a subsequent dose 7 hours after the first dose just after 3am of approximately 2mg tipped the effect over my comfort level and had me feeling uncomfortably paranoid and anxious, 300mg of mebicar (adaptol) rather than my usual 150mg second dose of the day knocked it on the head brilliantly.
coming up my planned time for sleep at about 6-7 hours before my 3am start (rain may dampen the plans for the daily 16km bicycle ride) and feeling distinctly like sleep will be possible, despite the indiscretion about the somewhat redose with 2mg at 10:30am - which is about 10 hours ago. fingers crossed.
update:
0454hrs: sleep did not come as readily as would have been liked, but a 10mg loratadine sorted that out and 4 hours was achieved, a theory is developing. not particularly good.
at about 0315hrs approximately 1.8mg was insufflated followed 10 minutes later by another 1.8mg. only at about perhaps 0415hrs did a significant and useful effect seem to set in, but being that in the interim i had ridden about 8 or 9km on my bicycle i can't say for certain whether this was not simply the onset of natural endorphin release or a metabolic byproduct.
pharmacological theorising:
1. an immediately active effect of the desoxy is a what appears to be mostly selective histamine 3 receptor agonism. that there is H3 activity is in no doubt whatsoever as every known alerting agent or insomnia causing drug known thus far has strong histamine 3 activity. it is also reported in this thread at least once an incident of histaminergic reaction to this chemical suggesting it is somewhat unselective, and if i remember correctly the reaction was immediate suggesting this is a direct effect of the chemical itself.
2. around 45 minutes after absorption, or so, a secondary effect begins which appears to be where the 'fun stuff' begins, and this effect seems to build up and remains until about 8-10 hours after dosing. i am starting to get an impression that there is definitely an active metabolite involved, if not more than one perhaps several, and this effect is shorter lived and its benefits are outweighed by the longer lasting H3 agonism previously hypothesised.
i'm not sure what measures are suitable for immediate counteracting of the H3 - i did find loratadine worked and it's one of the least sedating histamine antagonists. also i have had most of my life a set of symptoms which suggests an above average level of histamine activity, evidenced by short sleep periods, excessive body temperature, excess mucus, excessive saliva (possibly may be a factor in my good dental health despite my abject neglect), and a number of other symptoms described here
http://www.diagnose-me.com/cond/C447056.html now while i am somewhat skeptical of this diagnosis and the disease in general i can say for certain that these symptoms definitely can be attributed to histamine activity.
and so, it appears that the most direct and effective method of bringing sleep with desoxypipradrol is antihistamines. if anyone could suggest one with low toxicity and high selectivity for H3 antagonism it would be the trick to making the drug manageable. the effects on peripheral adrenalin and central noradrenalin and dopamine are fairly mild, and seem to have an 8-12 hour duration after which point they probably would not cause significant depletion of sleep quality. being that i have generally got away with 6 hours a night (more often than not i seem to wake up at exactly 6 hours after falling asleep unless i am sick or drank a lot of alcohol) and that it does not seem to greatly impair my overall health (while i do have high sinus mucus production i don't have poor immunity and have had the flu maybe twice and a third time most recently i stopped it dead in its tracks with increased fluids, antioxidants, echinacea, zinc and rest - my skin and overall complexion have the appearance to most people of being of a person in their mid 20s rather than early 30s), so long as the histamine antagonism is selective for H3 and is easily eliminated within 8 hours i don't see why i can't for the time being continue the use of desoxypipradrol.
however i would love to find out what the metabolites are if i could somehow and i am going to find out where and how much it costs to get an assay of urine metabolites and anything in the MW range of desoxypipradrol i would like to get the chemical formula if not the molecular model discovered.
or perhaps this has already been done and someone with access to medline or some such database can find out what are the known metabolites. my suspicion is that it is some kind of hydroxylated derivative, but of course not hydroxylated on the central carbon, although it seems likely that this is possibly one of the metabolites (pipradrol) as the wriggly structure of piperidine and polarity of the amine and its proximity may make it a major metabolite.
in any case, clearly the best antidote for the insomnia is an antihistamine. this may make this chemical not particularly useful. if, however, the more strong dopaminergic effects are from a metabolite other than pipradrol, it would be very useful to find out what it is and if it can be easily made from the parent compound as it would be the useful element amongst the useless crap that is caused by desoxypipradrol.
note: this does suggest the use of quetiapine (seroquel) as it has antihistamine activity - of course this also suggests tricyclics as well.
note 2: looking at it it appears that my idea about H3 receptors is precisely opposite from what is known, and perhaps this implies that desoxypipradrol has selective H3 antagonism, although that's entirely debatable at this point. antagonising H3, however, would take the reins off its effect on limiting monoamine activity. clearly the histamine aspect of the effect is only part of the story but the fact that loratadine permitted effective suppression of the alerting effect may still be helpful.
more observation and combinations are needed. this morning no adjuncts were taken and the sympathetic effects seem bearable but the anxiety is present so mebicar will dosed at 300mg to see if it's overtly beneficial effect noticed previously at this dose recurs.
1103hrs:
i am starting to understand how people find this stuff difficult to figure out. first 6 hours generally sucks, not sure exactly how to describe it, but it's basically unpleasant and distracting and all these sympathetic effects and - well ok i'm a bit lost how to describe it other than unpleasant. but then after a while it gets better. today so far i've put 50mcg of clonidine, 600mg of mebicar, 80mg of verapamil and 10mg of loratadine on top of it and now i feel fine and i am lost for an explanation as i had already dosed the mebicar and clonidine less than 2 hours after the first ~3.6mg no good, the second 300mg of mebicar, some loratidine, i find it highly doubtful it's the mebicar by itself, and the timelines of dosing of the adjuncts is starting to make me think there definitely is an active metabolite that does not take effect until about 6-8 hours in. only way for me to determine this positively would be to not take anything else (aaaargh the pain!) and see if it abates at that point. seems that what should definitely be doing something definitely isn't.
i wish i could get some clear confirmation of the nature of its metabolites. primary activity plus a slow buildup of an active metabolite would absolutely explain the effects.
ah! ok, it was mentioned earlier in this thread that storing it in water caused it to change colour but no apparent change in potency - the colour change suggests a possible polymerisation reaction, implying an oxidation something along the lines of the reactions described in here
http://books.google.com.au/books?id...=X&oi=book_result&resnum=6&ct=result#PPA52,M1 (google books thing of a book about lactam polyamides) which shows on page 52 the reaction mechanics of lactam in water. it involves the lactam adding on to an already fully ring opened and oxidised lactam (the diphenyl amino acid that results when the piperidine ring is opened by oxidation - requires 3 oxygen atoms, from the piperidine to the lactam to the aminoalcohol to the acid) would form a linear chain with diphenyls attached at every 6 carbons in the chain.
the only possible explanation for this degradation without the obvious concurrent loss of potency is that one of the intermediates in the oxidative decomposition in this process is more potent than the original chemical and has substantially similar effects (which i am thinking may not be similar to me because in general my reactions to stimulants is uncommon). the potency increase would have to be substantial also, at least 2x as strong if not more so. obviously a more conclusive understanding would require a lot of chemistry and chomatography, simply understanding this decomposition in water would lead to a lot more information.
seems likely though, that activity of the decomposition product would be substantially shorter, and perhaps not be a one dose a day drug, maybe on par with the T1/2 of meth.
just for shits and giggles i got some 3% peroxide and a tiny bit of desxoypipradrol (maybe 10mg), let it boil up until it acquired a 'light butterscotch' colour, then added some sodium bicarbonate and boiled it down until well past dry and inhaled the (funky) vapours. was just a qualitative test to see if, when oxidised quite extensively (the colour of the solution was a dark honey colour before freebasing it) had a noticable difference in effects for me. it does, more warm, relaxed feeling not so much of the cold tense wired feeling i get 10 minutes after insufflation. far from conclusive but enough to make me seriously consider means to alter either the chemical or my metabolism of it somehow. the trick would be oxidation with something to inhibit the polymerisation. or to accelerate the oxidation while it is being absorbed perhaps.
and for scientific theory justification purposes, finding a means by which the oxidatively opened piperidine ring by known mechanisms could be decarboxylated.
20090219 0634hrs:
took 4mg dexchlorpheniramine at 2100hrs last night, was probably too much antihistamine, next time i'll only take 2mg. worked effectively at allowing me to sleep, i was a bit too affected by it so didn't properly sleep until midnight and woke at just before 6 so finally some decentish amount of sleep. decided to have a day off the hard exercise, all my muscles are sore and probably not recovering as fast as they could if i was sleeping more and taking glutamine supplements.
today a strict dosing regime, ~4mg IN and for the purposes of examining the hypothesis discussed above no adjuncts whatsoever. i want to see if there indeed is a distinct change of character of the effects at around T+8hrs.