What is Accutane?

Accutane is a form of vitamin A. It reduces the amount of oil released by oil glands in your veneer, and helps your graze renew itself more speedily.
Alsou Accutane is prescribed for the treatment of wicked, disfiguring cystic acne that has not cleared up in retort to milder medications such as antibiotics. It works on the oil glands within the overlay, shrinking them and preventing deviant hardening of the skin.
Isotretinoin has been used to treat other skin disorders, including keratosis follicularis, pityriasis rubra pilaris, lamellar ichthyosis and leukoplakia.


Accutane is used for.
Treating critical acne in patients who do not pity to other medicines. It may also be in use accustomed to for other conditions as unhesitating by your doctor. The antiacne significance can last even after you be struck by finished your advance of medication.


Before using Accutane.
Some medical conditions may interact with Accutane. Certain your doctor or pill roller if you have any medical conditions, predominantly if any of the following apply to you: if you are in a family way, planning to become parturient, or are breast-feeding if you are alluring any prescription or nonprescription physic, herbal preparation, or dietary augment if you have allergies to medicines, foods, or other substances if you are broad and unable to use 2 effective forms of origination control or avoid carnal intercourse if you have diabetes, a children history of diabetes, grand blood cholesterol or triglyceride levels, psychiatric disorders, suicidal thoughts, liver cancer, pancreatitis, a bone breakdown condition (eg, osteoporosis), decreased bone density, an eating scramble, severe diarrhea, rectal bleeding, hearing problems, ringing in the ears, or desire pain.


How to use Accutane.
Take Accutane two times a day with a meal, unless your doctor tells you otherwise. Swallow the capsule. Don't suck or chew it. Take it with a full glass of water, milk, or other nonalcoholic liquid.
Accutane comes with an extra patient information sheet called a Medication Guide. Read it carefully. Read it again each time you get Accutane refilled.

Take Accutane by mouth with food.
Scuttle the capsule with a entire glass of water or other transparent. Do not break, crush, munch, or suck on the capsule in front swallowing. This leave help prevent the medication in jail the capsule from irritating your throat. For most talented results, take Accutane regularly.

You bequeath get no more than a 30-day afford of Accutane at a time to be unwavering you check in with your doctor each month to argue side effects. If you slip a dose of Accutane , guide it as soon as possible. If it is verging on time for your next amount, skip the missed measure and go back to your fortnightly dosing schedule. Do not stomach 2 doses at once.

After you winding up taking Accutane, there should be at least a 2-months "take one's repose period" during which you are off the psychedelic. This is because your acne may at to get better even while you are no longer taking the medication. Right away the 2 months are up, if your acne is to severe, your doctor may hope for to give you a second way of Accutane. If you are still growing, your doctor may commend a longer "rest space."

What should I converse about with my healthcare provider once taking Accutane?
Accutane is accessible only under a bosom program called iPLEDGE. You have to be registered in the program and flag documents stating that you twig the dangers of this medication and that you concede to use birth control as required by the program. Accutane can occasion severe, life-ominous birth defects if the natural takes the medication during pregnancy. Equivalent one dose of Accutane can justification major birth defects of the pet's ears, eyes, look out on, skull, heart, and perspicacity. Never use Accutane if you are charged.
Women of child-bearing potential should agree in writing to use two exact forms of birth switch and have regular pregnancy tests previous to, during, and after fetching Accutane. Unless you must had a total hysterectomy or participate in been in menopause for at least a year, you are considered to be of stripling-bearing potential.

If you organize certain conditions, you may lack a dose adjustment or one of a kind tests to safely apprehend this medication. Up front taking Accutane, aver your doctor if you are allergic to any foods or drugs, or if you attired in b be committed to:
a personal or family history of depression or mental illness;
heart disease, high cholesterol or triglycerides;
osteoporosis or other bone disorders;
diabetes;
asthma;
an eating disorder (anorexia nervosa); or liver disease.


Possible side effects of Accutane
Accutane may effect drowsiness or dizziness. These effects may be worse if you haul it with alcohol or a sure thing medicines. Use Accutane with admonition. Do not drive or perform other at all unsafe tasks until you recognize how you react to it. A surprising decrease in night hallucination may occur while you are delightful Accutane . Use caution when driving at Cimmerian dark and avoid driving at sundown if you experience decreased eventide vision. If you abrade contact lenses, you may be enduring difficulty wearing them during and after analysis. Do not give blood while attractive Accutane and for 1 month after stopping intriguing Accutane. Do not pledge alcohol while entrancing Accutane.

Worsening of acne may come to pass during the first leave of therapy. This does not present failure or a need to end the medicine. To inhibit cracking of lips, use a lip moisturizer or balm. Do not entertain cosmetic procedures to flat your skin, including waxing, dermabrasion, or laser procedures, while you are intriguing Accutane and for at least 6 months after you plug up. Accutane can increase your time of scarring from these procedures. Accutane may issue you to become sunburned more undoubtedly. Avoid the sun, sunlamps, or tanning booths until you recognize how you react to Accutane. Use a sunscreen or weary protective clothing if you have to be outside for more than a discourteous time.

All medicines may occasion side effects, but varied people have no, or paltry, side effects. Hindrance with your doctor if any of these most Non-private side effects persist or turn bothersome:

Abnormal hair growth; abnormal skin sensations; bleeding and redness or swelling of the gums;changes in menstrual flow; chapped lips; decreased tolerance to contact lenses; dizziness; dry eyes and mouth; dry nose that may lead to nosebleeds; dry or peeling skin; fatigue; flushing; general body discomfort; hair thinning; headache; itching; lack of energy; nervousness; respiratory tract infection; sleeplessness; sweating; temporary worsening of acne; voice changes.

Read more about Accutane for Acne

Reboxetine; Adrafinil; Modafinil

Reboxetine (Edronax) is a well-tolerated , highly selective "noradrenergic" agent. Crudely, whereas serotonin plays a vital role in mood, noradrenaline is essential to maintaining drive and the capacity for reward. There's a fair bit of evidence that chronically depressive people have dysfunctional and atypical noradrenergic systems - particularly their alpha 2 and beta-adrenoceptors. Reboxetine itself doesn't have the disruptive effects on cognitive function or psychomotor performance so annoyingly typical of older clinical mood-brighteners. Indeed the new NorAdrenaline Reuptake Inhibitors (NARIs) are probably under-used and under-hyped. NARIs - and dopaminergics like amineptine (Survector) - may be especially good for drive-deficient "anergic" states where the capacity for sustained motivation is lacking; and for melancholic depressives with a poor ability to cope with stress. Perhaps surprisingly, preliminary studies suggest reboxetine can actually reverse tranylcypromine-induced hypertensive crises. The "cheese effect" is usually triggered by ingesting tyramine-rich foods. Thus NARIs plus MAOIs may prove a potent form of combination-therapy.

Depressive hypersomniacs who fare poorly on SSRIs, or can't get hold of amineptine or EC-licensed reboxetine, might consider trying a so-called eugeroic ("good arousal") agent instead; more adventurous souls may wish to combine the two. Alpha-1 adrenergic agonists like adrafinil and modafinil are centrally-acting stimulants which can brighten mood and sharpen mental focus. They stimulate the noradrenergic post-synaptic receptors and thereby boost alertness, activity and energy. At sensible dosages, they are remarkably free of side-effects. However, the approval process in the USA is so slow, costly and bureaucratic, and the marketing hurdles typically so formidable, that foreign companies are often deterred from seeking FDA acceptance. [modafinil was licensed by the FDA as Provigil for the treatment of narcolepsy in Dec 1998 ] So elderly people continue to suffer the prescription of mildly dementing anticholinergics like the dumb-drug tricylcic imipramine. Adrafinil, by contrast, is at least as successful as hepatotoxic Anglo-Saxon products at treating the cognitive and memory impairments of incipient senility.

Fortunately, a "French" drug like adrafinil can now be ordered over the Net; but it ought to be available at the local corner store. It has the commercial disadvantage of being very cheap.

Bupropion; Amineptine

Bupropion (Wellbutrin) is possibly less effective than nomifensine. Yet it's useful because it lacks the adverse effects on sexual function characteristic of the SSRIs. In some subjects, in fact, libido, arousal, and the intensity and duration of orgasm may actually increase. Bupropion mildly blocks the reuptake, but diminishes the release, of dopamine. This may account for reports of its diminished propensity to induce mania in the genetically susceptible. Its active metabolites block the reuptake of noradrenaline. Chewed as a gum, bupropion is good for giving up smoking. Scandalously, it isn't licensed and marketed in Europe.
Amineptine (Survector) is a clean-ish, (relatively) selective dopamine reuptake blocker. Higher doses promote dopamine release too. Amineptine is liable occasionally to cause spontaneous orgasms. It is a mild but pleasant psychostimulant and a fast-acting mood-brightener. Unlike other tricyclics, it doesn't impair libido or cognitive function. Unlike typical stimulants and other activating agents, it may actually improve sleep architecture.
Scandalously, amineptine isn't licensed and marketed in Britain and America. For it is feared it might have "abuse-potential".

Methylphenidate; Minaprine; Nomifensine

A SSRI can be combined ("augmented"; sounds more soothing to the official medical ear) with a dopaminergic such as methylphenidate. As "Ritalin", methylphenidate is prolifically dispensed to American schoolchildren for different purposes altogether. In spite of its structural relationship to amphetamine, methylphenidate resembles in many ways a benign version of cocaine, yet with a much longer half-life. It blocks the reuptake, but doesn't significantly release, the catecholamines noradrenaline and dopamine. If it is combined with an SSRI, all of which have anti-obsessive-compulsive properties too, the likelihood of dose-escalation is minimised.
Chewing coca leaves with a dash of powdered lime is a nutritious and energising way to sustain healthy mood.
Unfortunately, it is not very good for one's teeth.
A more cautious but still interesting option might be minaprine. Minaprine blocks the reuptake of both dopamine and serotonin. It is also in some degree cholinomimetic. Thus it may exhibit both mood-brightening and nootropic properties. Much more research is needed.
Nomifensine (Merital) showed great promise as a pleasantly stimulating dopaminergic which also inhibits the reuptake of noradrenaline and - to a much lesser extent - serotonin. It was withdrawn from licensed use after the discovery of its rare side-effect of precipitating a serious blood-disorder. For retarded melancholics, however, it was typically a very effective and well-tolerated mood-brightener with minimal side-effects. The risk/reward ratio of its carefully-monitored use may have been misjudged.

Dopamine function

What's missing, crucially, is vigorous and prolonged stimulation of meso(cortico-)limbic dopamine function.
This is really much more fun than it sounds. The currently available experimental evidence has persuaded many - but not all - researchers that the mesolimbic dopamine system serves as the final common pathway for pleasure in the brain. Enhanced responsiveness of post-synaptic dopamine D2/D3 receptors is crucial to long-term emotional well-being. The otherwise anomalous mood-brightening effects of the serotonin-reuptake accelerator tianeptine, for instance, are probably explained by its tendency to increase extracellular concentrations of dopamine in the nucleus accumbens. All "serotonergic" and "noradrenergic" mood-brighteners eventually act on the mesolimic dopamine pathway, albeit in differing degrees and with varying delay. And new anti-Parkinsonian and anti-Alzheimer's agents, notably roxindole and pramipexole, owe their exciting potential role as fast-acting antidepressants to their dopaminergic action.
The full story is inevitably complex. Dopamine isn't itself the magic pleasure-chemical, though its functional role is crucial. Researchers into affective disorders readily get over-attached to a particular neurotransmitter, its receptor sub-types and their signal transduction cascades. Traditionally, serotonin and noradrenaline have attracted the fiercest rival partisans. "Dopaminergic" (and opioid) agents, by contrast, are suspect. They are politically incorrect since they are both potentially "abusable". Moreover safe and sustainable empathogens are arguably as morally urgent as safe and sustainable mood-boosters. At any rate, mesolimbic activation, exclusively or otherwise, enhances the intensity of experience; increases pleasure and libido, and boosts cognitive performance. Even better, certain dopamine-enhancing drugs may have neuro-protective properties too.
So what are the other contemporary options for chemical life-enhancement?

Recreational drugs

The commonly recognised legal and illegal recreational drugs offer poor prospects for sustained biological mood-enhancement. So what about the heterogeneous group of compounds uninvitingly labelled as anxiolytics and antidepressants? Have they potentially anything significant to add to most people's quality of life? Official medical doctrine says no. Allegedly, only sufferers from clinically-sanctioned psychiatric disorders will benefit from such agents; though in recent years it has at last been formally recognised that depressive disorders are under-diagnosed and under-treated even by the twentieth century's abjectly poor standards of acceptable ill-being. Most of humanity, however, still doesn't fit any of the official diagnostic boxes. Can "diagnostic creep" triumph over therapeutic minimalism and enhance their quality of life? Yes. Must the goal of pharmacotherapy be as limited as Freud's aspiration for psychotherapy: "to transform hysterical misery into common unhappiness"? No.

First, the boring but crucial preliminaries. Optimal nutrition and exercise will increase the efficacy of all the potential life-enhancers touted here. A rich supply of precursor chemicals (e.g. tryptophan, the rate-limiting step in the production of serotonin) can also reduce their effective dosages. By choosing to eat an ideal "stone-age" diet rich in organic nuts, seeds, fruit and vegetables, and drastically reducing one's consumption of saturated fat (red meat, fried foods), sugar (sweets etc) and hydrogenated oils (found in margarine and refined vegetable oils), then one's baseline of well-being - or at least relative ill-being - can be sustainably lifted. Visitors to HedWeb probably don't expect to be assailed by sermons on the benefits of exercise any more than food-faddism. Yet regular and moderately vigorous physical exertion releases endogenous opiates, enhances serotonin function, stimulates nerve growth factors, and leads to a livelier, better-oxygenated brain.

Alas, clean living and wholesome thoughts typically aren't enough. We need stronger medicine to flourish. At first glance, however, the standard, State-rationed chemicals aren't a brilliant bunch.
The so-called minor tranquillisers, the benzodiazepines such as diazepam (Valium) and the shorter-acting temazepam, are sometimes useful but still dreadfully crude anti-anxiety agents. They act primarily on the GABA (gamma aminobutyric acid) receptor complex. GABA functions as the main inhibitory neurotransmitter in the central nervous system. The progress of molecular biology and neurogenetics in unravelling the fiendish complexity of GABA's receptor sub-types should eventually allow more targeted compounds to be developed. These more selective and site-specific drugs will lack the sedative and hypnotic properties of today's marketed brands. In the meantime, benzodiazepines in current use tend to induce dependence, dull consciousness and impair the intellect. So there's not much chance of radical life-enrichment here.

Buspirone (Buspar), is somewhat more promising. It acts on an autoreceptor subtype of serotonin. This means it has mood-brightening properties too; and hence it is useful in anxious depressive states. Buspirone lacks the intellect-clouding effects of other clinical and alcoholic anti-anxiety agents. Yet its weak and equivocal effects on sub-types of dopamine function, while useful for the purposes of commercially touting its lack of "abuse potential", mean it isn't very exciting or especially effective.

The so-called anti-depressants fall into several categories. Their mood-brightening effect is correlated with alterations in the concentration of catecholamines and/or serotonin in the central nervous system and the long-term receptor re-regulation these changes provoke.
The tricyclics, prototypically imipramine (Tofranil), and their allies are relatives of the neuroleptic drug chlorpromazine. Chlorpromazine is also known as Largactil, the notorious "chemical cosh". Tricyclics block to varying degrees the reuptake of serotonin and noradrenaline into the nerve cell terminals from where they are released. Perhaps unsurprisingly given their parentage, they are all dirty drugs, though some are dirtier than others.
Their anti-cholinergic effects harm memory and intellectual performance. Their anti-histamine action induces drowsiness and sedation. Their adverse effect on cardiac function makes them dangerous in overdose. Most "euthymic" volunteers on whom they have been tested don't like their dulling effects of consciousness. Unlike chlorpromazine, the tricyclic antidepressants don't noticeably block the dopamine receptors. But with one notable exception, they do precious little to stimulate dopamine function either. Hence they're not much fun even for the severely depressed people who can benefit from taking them. For three decades they were the mainstay of the treatment of clinically-acknowledged depression. They contributed to the widely-held medical opinion that anything classed as an antidepressant won't help "normal" people; unless of course they were "really" depressed. Basically, tricyclics are cheap, nasty and best avoided.
Much better, but still in some ways deeply flawed, are the selective serotonin reuptake inhibitors.
Serotonin, "the civilising neurotransmitter", plays a vital role in mood, memory, appetite, sleep, pain perception and sexual desire.

Fluoxetine (Prozac), fluvoxamine (Luvox), paroxetine (Paxil), sertraline (Zoloft), and citalopram (Cipramil, Celexa) are currently licensed and marketed. More of their "me-too" relatives are on the way from pharmaceutical companies eager for a lucrative piece of the action. The SSRIs all differ in their half-lives, chemical structure and precise specificities. Their functional effects are broadly similar. Their mood-brightening, resilience-enhancing and anti-anxiety properties really can make a modest percentage of the population feel "better than well". As a class, they don't have the physically unpleasant and cognitively debilitating anti-cholinergic effects of the tricyclics. A much larger section of the community - folk who daily knock back huge quantities of ethyl alcohol in the socially accepted fashion - could surely gain from the durably enhanced serotonin function SSRIs can yield. Such a switch would necessitate a big change in marketing strategy.

The beneficent properties of the SSRIs are celebrated in Peter Kramer's contemporary classic Listening to Prozac. Kramer has written a remarkably honest book. It's a discursive memoir by a therapist who is forced to admit that many of his clients seemed rapidly to fare far better on a pill than on his industrial-strength regimen of caring talk-therapy. Kramer's discussion of "cosmetic psychopharmacology" and "designer personalities", however, enraged traditionalists. For chemical Calvinist orthodoxy finds the notion that people should have a right pharmacologically to choose who and what they want to be profoundly offensive.

Two common problems limit the usefulness of SSRIs, at least when taken on their own. The problems stem from the indirect inhibitory effect of Prozac-style drugs on dopamine function, a consequence of deliberate selective targeting on the functional enhancement of subtypes of serotonin pathway.

First, SSRIs can compromise libido and sexual performance. This isn't always a disadvantage in over-excitable young males. It can still be a very distressing phenomenon for people too embarrassed to talk about it. Technical performance difficulties can sometimes be counteracted by taking (the alpha-2 adrenergic agonist) yohimbine; the phosphodiesterase inhibitor sildenafil (better known as the sexual rocket-fuel Viagra); or a dopamine agonist, licit or otherwise, before bedtime action. Yet this is scarcely an ideal solution.

Second, though some subjects may feel mildly euphoric, in other users the SSRIs serve more as mood-stabilisers and -flatteners in their lives. By increasing the user's emotional self-sufficiency, too, SSRIs may subtly change the "balance of power" in personal relationships - for good or ill. In some cases, SSRIs may even act as thymoanaesthetisers which diminish the intensity of felt emotion; by contrast, a mood-brightening serotonin reuptake-enhancer like tianeptine may intensify emotion instead. Affective flattening may be welcome to someone in the pit of unmitigated clinical depression. It is scarcely a life-enriching property for "normal" people who lack any convenient diagnostic category which acknowledges their malaise.

Some dead drugs

One spectacularly incompetent route to a lifetime of happiness involves taking illegal psychostimulants such as cocaine or the amphetamines. In the short term, their activation of the sympathetic nervous system tends to elevate mood, motivation and energy. Users tend to talk a lot. Self-confidence is enhanced: these are "power drugs". Physical strength and mental acuity are variably increased. Whereas cocaine blocks the neuronal re-uptake of the catecholamines (noradrenaline; dopamine), amphetamine triggers to a much greater extent their synaptic release as well. It is thus more potent.
In either case, libertarian indignation that the State presumes to subject its citizens to totalitarian-style mind-control should not obscure the fact that for most purposes these are not useful drugs. This is because the central nervous system supports a web of mutually inhibitory feedback-mechanisms. In response to a short-term increase of mood-mediating monoamines in the synapses, the genes and neuronal receptors re-regulate. So at best no real long-term benefit is derived from the use of such compounds. Neither cocaine nor amphetamine yield the sustained activation of intracellular signal-transduction cascades needed to cheat the hedonic treadmill.

Some people continue to take psychostimulants casually for years without serious harm. Yet the potential risks of adverse physical, psychological and social ill-effects are high. Hence their use is best discouraged.
The depressant opioids are marginally more benign. They can be extremely pleasurable. Next century, their customised and site-selective successors may play a valuable role in promoting emotional superhealth. We could all do with having our native endorphin systems enriched. Unfortunately, the present crop are physiologically addictive They lose quite a bit of their euphoriant effect as tolerance sets in. Typically, they inspire a dreamily contented disengagement from the problems of the world. They diminish any drive to constructive activity. Sadly, too, their use impairs the release of endogenous opioids normally induced by social interaction with friends and family.

The physical risks of opioid use shouldn't be exaggerated. Most of the problems that users suffer ultimately derive less from their choice of drug itself than from the illegal status of exogenous opioids in contemporary society. Yet even if they were legal and given away in cereal packets, they wouldn't make a good choice of mood-booster - or at least not in their present, crudely non-specific guise. kappa- agonists, for instance, have dys phoric and psychotomimetic effects; one might as well drink ethyl alcohol spiced with meths. The paradise-engineers of posterity will surely weed out such adulterants from their elixirs altogether.

By contrast to today's opioids, marijuana isn't usually addictive in the traditional sense of the term. It can, however be habit-forming. It has euphoriant, psychedelic and sedative properties. Experiments with stoned rats suggest the drug reduces the amount of corticotrophin-releasing factor in the amygdala. Excess secretion of CRF is associated with abnormalities in the HPLA axis and depression. The rebound surge of CRF on ceasing cannabis-use is associated with increased vulnerability to stress and a withdrawal-reaction; arguably one good reason not to stop in the first instance.

The primary psychoactive ingredient in marijuana is THC, tetrahydrocannabinol. Smoking or eating marijuana and its complex cocktail of compounds may rarely trigger episodes of depersonalisation, derealisation and psychosis. Sometimes it can induce paranoia, particularly in advocates of The War Against Drugs. More commonly, it just leaves the user pleasantly and harmlessly stoned. It's fun. Sleepiness, pain relief and euphoria are typical responses. Indeed the first brain-derived substance found to bind to our cannabis receptors was christened "anandamide", a derivative of the Sanskrit word for internal contentment. Getting high may thus serve as an innocent recreational pastime in an uncaring world.

Yet marijuana is not a wonderdrug. Cognitive function in the user is often impaired, albeit moderately and reversibly. Marijuana interferes with memory-formation by disrupting long-term potentiation in the hippocampus. It seems that one of the functions of endogenous cannabinoids in the brain is to promote selective short-term amnesia.
Forgetting is not, as one might have supposed, a purely passive process. Either way, choosing deliberately to ingest an amnestic agent for long periods is scarcely an ideal life-strategy. It's especially flawed given the centrality of memory to human self-identity. Some artists and professional bohemians, it is true, apparently do find smoking grass an adjunct to creative thought. For persons of a more philistine temperament, on the other hand, it's hard to see such a drug as a major tool for life-affirmation or the self-development of the species. This does not, one ought scarcely need to add, suggest users should be persecuted and criminalised.

The empathogen "hug-drug", ecstasy (methylenedioxymethamphetamine; MDMA) offers a wonderfully warm, sensuous, loving, and empathetic peak experience to the first-time user. Distrust, suspicion and jealousy evaporate. They are replaced by a serene sense of universal love. The sensorium remains clear. Emotion is intensified. Much recreational drug-use tends to be self-centred. It is often branded as selfish. Yet here is a "penicillin of the soul" which promises to subvert our selfish-DNA-driven tendency to self-aggrandisement.

Disappointingly, whether due to enzyme-induction or other causes not fully understood, most users never fully recapture the magic of their first few trips. Moreover ecstasy is neurotoxic to serotonergic axons. It may even be harmful at sub-therapeutic doses. As the uncertain process of neural recovery sets in, heavy users in particular may experience the subtle long-drawn-out reversal of all the good effects they initially enjoyed from the drug. Taking a post-trip selective serotonin re-uptake inhibitor (SSRI) such as fluoxetine (Prozac) 2-6 hours afterward is prophylactic against the measurable post-E serotonin dip otherwise experienced some 48 hours later. Yet taking SSRIs on a regular basis largely nullifies the already attenuated benefits of prolonged ecstasy use. In any case, the duration of the peak experience is a mere 90 minutes. So taking ecstasy scarcely amounts to a full-scale strategy for life either. It does, on the other hand, deliver an exquisite foretaste of the beautiful forms of consciousness that ultimately await us.

Another tantalising and deliciously sensuous hint of the sublime is offered - infrequently and unpredictably - by gamma-hydroxybutyric acid (GHB). GHB usually takes the form of a clear, odourless, slightly salty-tasting liquid.
It's also an endogenous precursor and metabolite of the inhibitory neurotransmitter GABA. GHB is non-toxic; but it mustn't be mixed with alcohol or other depressants. It's metabolised quickly to carbon dioxide and water. GHB's steep dose-response curve means naive users run the severe risk of falling asleep. When used lightly in recreational rather than stuporific or anaesthetic doses, GHB is a touchy-feely compound which typically induces deep muscular relaxation, a sense of serenity, and feelings of emotional warmth. Often it enhances emotional openness and the desire to socialise. Tactile sensitivity and the appreciation of music are enriched. Most remarkably, the moderate user may awake refreshed after a deep restful sleep: GHB appears temporarily to inhibit dopamine-release while increasing storage, leading to the brightened mood and sharpened mental focus of a subsequent "dopamine-rebound". GHB acts both as a disinhibitor and an aphrodisiac. The intensity of orgasm is heightened. Hence GHB is potentially useful in relieving the psychopathologies of prudery and sexual repression. Unfortunately, its therapeutic value has been eclipsed by its demonization in the mass-media. Stories of chaste virgins turning into sex-crazed nymphomaniacs make great copy and poor medicine. Moreover GHB is sometimes confused with the amnestic "date-rape" benzodiazepine, flunitrazepam - better-known as the potent and fast-acting sedative-hypnotic "forget pill", Rohypnol. Bought on the street, GHB may be confused with all sorts of other substances too.

Yet even pure GHB is no magic elixir. Not everyone likes it. GHB's psychological effects are unpredictable and poorly understood. Nausea, dizziness, inco-ordination are common; reaction-time is slowed. GHB does not usually promote great depth of thought. Its very status as "an almost ideal sleep inducing-substance" makes it of limited use to those who aspire instead to be more intensely awake. The lack of any discernible body-count to fuel the periodic moral panics its use induces may allow a partial rehabilitation. Yet GHB evokes - at best - only a faint and fleeting parody of the life-long chemical nirvana on offer to our transhuman successors.

Alcohol - the traditional date-rape drug of choice - and, most insidiously of all, cigarettes are the really sinister mass-killers. With that poker-faced Alice-In-Wonderland logic popular amongst the world's sleazier governments, not merely do the authorities preserve the legal status of cigarette sales here in the UK on grounds of upholding personal liberty. The slickly expensive marketing and glamorisation of tobacco products to potential victims is sanctioned on similar grounds too. We ought to be as shocked at tobacco promotion as we'd certainly feel if instead the billboards urged kids to try heroin because it's cool. Yet familiarity breeds moral apathy. Youngsters are typically hooked before they are in any position to make an informed choice of poison - or even to abstain altogether.

Meanwhile a state-supported export drive targets the poor in vulnerable Third World countries. With a cynicism that almost beggars belief, one celebrated ex-British Prime Minister accepted a million-dollar bribe from a leading member of the drug-cartels for her services. Her party's ineffable Home Secretary then delivered himself of blood-curdling calls for a crack-down on evil drug-pushers(!). He went on to increase the draconian penalties already available for personal users of cannabis.

So long as our governments collude with the organised drug cartels to share out the billions of dollars of tax revenues mulcted from nicotine-addicts - thereby keeping direct taxes visibly down and themselves visibly in office - there seems little hope of a more intelligent approach to psychoactive drugs as a whole.