- This topic is empty.
-
Posts
-
This is David Pearce dairy. David Pearce write the best articles about brain functions. For him, the best way to improve dopamine enhancement is amineptine with selegiline. 20 year’s ago my physician give me survector (amineptine). This is for me the best drug for dopamine enhancement, no crash like ritalin or nicotine…
But Servier stop the production fews year’s ago.David Pearce article
100 mg amineptine (Survector) and 2 x 5 mg selegiline (l-deprenyl, Eldepryl) daily. I also take omega3-rich flaxseed [linseed] oil supplements; LEF’s “Life Extension” mix; and resveratrol with quercetin. And that’s it – for now, at least.Amineptine increases exploratory behaviour in rats. Since taking it, I have been seized by a desire to travel the world. Climbing volcanoes in Indonesia, exploring Machu Picchu, and communing with giant tortoises in the Galapagos Islands are adverse side-effects not reported on the product label. When at home in England, I spend my days webmastering for the abolitionist project [my raison d’etre]; rocking autistically to pop music on my iPod; or pushing back the frontiers of knowledge in Borders’ bookstore Starbucks café – the haunt of Brighton’s movers-and-shakers, its resident conspiracy theorists, and anyone who needs a library that serves industrial-strength black coffee.
In spite of its dopaminergic action, I almost never bothered to try amineptine in the first place. Not being a chemist, I assumed it would have dumb-drug antimuscarinic effects in virtue of its being a tricyclic. Amineptine is also devilishly difficult to obtain. Colourful tales of King Rat, double-dealing Brazilian lawyers, and a cast of characters plucked from a Tarantino movie are probably best omitted here. However, I seem to have emerged unscathed. In Rio, someone stole my vegetarian shoes while I was playing football on the beach; but anyone who needs to nick my shoes probably deserves them more than I do.
Missing footwear aside, I’ve now prudently stockpiled plenty of amineptine for a rainy day. Frustratingly, Servier halted production in Brazil in early 2005. So the global amineptine famine is now worse than ever. Amineptine’s ill-named abuse-potential i.e. the extremely mild euphoria that follows for an hour or so after ingestion, is weak and independent of its more subtle but sustained elevation of mood and motivation. As with nicotine or caffeine, amineptine users typically learn to self-titrate their intake for optimal effect: uncontrolled dose-escalation is rare and self-defeating. I guess that amineptine’s acute action might be mildly tempting to teenagers scouring the family home in vain for household products to swallow or sniff; but this was a childhood rite of passage I somehow managed to skip.
After Servier withdrew Survector in mainland Europe some years ago, amineptine.com received a stream of sometimes heart-rending emails from consumers, doctors and even pharmacists who told us it is was the only medication that worked: was there any way to obtain an alternative supply? [Occasionally, we still get similar plaintive emails from people who say the same about the long-vanished noradrenaline and dopamine reuptake inhibitor nomifensine (Merital).] Short of ordering amineptine as a “research chemical” via a chemical supply house, or synthesizing it via grandma’s bathtub chemistry kit, the answer was no. Even the usual grey-market pharmacy sources on-line dried up. This particular drug deficit was doubly frustrating here at BLTC HQ: Brighton is chemical capital of the UK, and if one wanted to score truckloads of class-A euphoriants or psychedelic exotica, then one could do so (I am told) within an hour. But sustainable mood-brighteners are thin on the ground. Until tomorrow’s designer genomes deliver invincible mental health for all, there is a pressing need for rationally designed psychotropics that are cheap, harmless and habit-forming. Admittedly, a marketing slogan on the lines of “Addictive By Design” isn’t the ideal rallying-cry for a novel life-enriching pharmaceutical in today’s prohibitionist climate. If I had a teenage daughter, I’d probably find myself chanting “Just Say No” too. But if a drug doesn’t make you want to take it again, then it probably isn’t any good – life-changing psychedelic epiphanies aside, and they might get disruptive every day of the week.
Alas amineptine itself is no panacea. On the contrary, it’s a dirty third-rate stopgap, yielding a rather one-dimensional kind of well-being suitable for a Darwinian world. A noradrenergic/dopaminergic drug regimen can lend a certain inner tension to the psyche; it also makes one less introspective and more outward-directed – something of a misnomer if one is only an inferential realist who believes that the so-called perceptual world is just a toy simulation each mind-brain runs. At any rate, amineptine is a useful agent only because current alternatives are so poor. One day, I hope to find something better. Most studies of mood-brighteners confound the response of anxious and/or agitated depressives with those who may be known, somewhat unflatteringly, as retarded melancholics. On this basis, amineptine isn’t statistically superior to other contemporary meds. For all the heady talk of pharmacogenetics and a new era of “personalised medicine”, drug companies are loathe to encourage “market segmentation” for fear of reduced profits. This reluctance is misplaced: melancholics in particular don’t do at all well on current drug therapies. Indeed prescription psychotropics are mostly so dire that anyone with a melancholic streak might be better served by a blend of old-fashioned Papaver Somniferum and coca leaves, despite their well-advertised pitfalls. Doctors bemoan the reluctance or inability of their patients to take their prescription meds as instructed; but this comes perilously close to blaming the victim. “Patient compliance” is so erratic because licensed “antidepressants” are often ineffective, side-effect-ridden or even actively depressogenic. Perhaps this dismal track-record isn’t surprising. Investigational drugs are tested to see if non-human animals will self-administer them and discarded if they do – arguably not the smartest heuristic for life-enhancement either for humans or our horribly abused cousins. Thus the so-called antipsychotics, for instance, frequently induce apathy, dysphoria and generally mess people’s heads up, albeit in ways that ensure their victims intrude less on the lives of others. As it happens, a neuroleptic/antipsychotic is one of the categories of drug I have never felt brave enough to investigate. Somehow I doubt if there will ever be a PiHKAL for antipsychotics: devotion to the experimental method has its limits. Once my capacity to do useful webmastering for the abolitionist project is spent, however, I dream idly about entering the Guinness Book of Records under the category of world’s greatest sustained euphoria – a form of record-breaking unaccountably missing from today’s roster of human achievement. Goodbye depressive realism; hello hedonistic bliss. Of course, it’s not going to happen; but I have fantasies of implanting stem cells and nerve growth factors into my stunted reward centres and expiring in my dotage from an uncontrolled proliferation of pleasure cells. Does this bespeak a lack of moral seriousness? Well, perhaps.
On a more sober note, I take selegiline at a higher dosage (2 x 5 mg daily) than is (probably) optimal for life-extension purposes. The aim here is maximal selective inhibition of MAO-B for improved mood and motivation; but it’s not MAO inhibition per se that accounts for selegiline’s neuroprotective role, but its propargylamine moiety. This is borne out by the neuroprotective action of the S isomer of rasagiline, even though it’s over 1000 times less potent as an MAO inhibitor. Selegiline, the older drug I’ve taken for most of the past decade, will soon be available at substantially higher and MAO-unselective dosages in the form of controlled-release EMSAM patch. Bypassing the gastrointestinal tract avoids the need for dietary restrictions. I will probably try EMSAM if my rasagiline experiment doesn’t work out, though only at a lower, relatively MAO-B selective dosage: agents with any kind of serotonergic action [unlike MAO-B, MAO-A also breaks down serotonin and noradrenaline] eventually make me listless. Instead, I need drive, exuberance, “life force”. Anything worthwhile in this world – and most of its horrors – has been achieved by larger-than-life characters, defying adversity to triumph over impossible odds. Unfortunately, I still undergo a catastrophe-reaction if one of my cacti dies or a friend wrinkles her nose in disapproval – not a good index of psychological robustness if one wants to save the world. Fortunately for victims of the syndrome in question, the Net offers hope to hormonally challenged, smaller-than-life characters, in theory at least.
As an experiment, I intend shortly to substitute the novel “second generation” MAO-B inhibitor rasagiline (Agilect, Azilect) for selegiline. There is negligible evidence that selegiline’s trace amphetamine metabolic by-products occur in sufficient quantities to exert any long-term adverse effects; but I would like to explore MAO-B inhibited life without them. Hence the attraction of Professor Youdim’s discovery. One reason for rasagiline’s lack of abuse potential/acute enjoyability may be the equivocal role of phenylethylamine (PEA). Several studies confirm PEA may have an antidepressant effect. It may serve as a [catecholamine] “enhancer”. Yet PEA can also act acutely as an endogenous anxiogen. This tallies with my own experience: a mild anxiety or inner tension – occasionally amounting to OCD-like symptoms – ensues very shortly after taking selegiline. Some subjects say they notice no subjective acute or chronic effects while on it. Others report a slight elevation of mood and alertness from the trace amphetamine metabolites some three hours or so after taking a tab. I most definitely fall into the latter category too; and I can’t believe it does me any long-term good.
- You must be logged in to reply to this topic.