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
THE DOPAMINE CONNECTION
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 - investigators 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. Insofar as they work, all "serotonergic" and "noradrenergic" mood-brighteners
eventually act on the mesolimbic dopamine pathway, albeit in differing degrees and with varying delay. New anti-Parkinsonian agents, notably pramipexole (Mirapex), ropinirole (Requip), and cabergoline (Dostinex) owe their potential role as fast-acting pro-sexual antidepressants to their dopaminergic action. Likewise, the possible mood-brightening effect of low doses of the dopamine
receptor antagonist amisulpride (Solian), more commonly considered an antipsychotic agent, is explicable because amisulpride preferentially blocks the presynaptic dopamine D2/D3 autoreceptors; dopaminergic
transmission is thereby enhanced.
The full story is inevitably complex. Dopamine agonists and reuptake inhibitors are often inadequate long-term mood-brighteners by themselves. The mesolimbic dopamine system mediates
reward-signalling, incentive salience and a sense of urgency and significance, not the essence of pure bliss. Dopamine isn't itself the magic pleasure-chemical, though its functional role in conjunction with glutamate and mu opioid agonists in regulating medium spiny neurons of the rostral shell of the nucleus accumbens is crucial. Researchers into affective disorders readily get over-attached to one particular neurotransmitter system, 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 potentially "abusable". Moreover it can be argued that the research and development of safe and sustainable
E-like empathogens and socialbilizers is as morally urgent as the license of safe and sustainable euphoriants. At any rate, enhanced mesolimbic dopamine release,
exclusively or otherwise, enriches the intensity of experience; increases pleasure and libido, and potentially boosts cognitive performance. Even better, whereas some dopaminergics are potentially toxic, some dopamine-enhancing agents may have neuroprotective properties as well.
So what are the other contemporary options for chemical life-enhancement?
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 taken in sustained-release form or combined with an SSRI, all of which have anti-obsessive-compulsive properties too, then 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 (Cantor). 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.
Merital (nomifensine) showed great promise as a pleasantly stimulating dopaminergic that also potently inhibits the reuptake of noradrenaline and - to a much lesser extent - serotonin. It was marketed by its manufacturers Hoechst with the slogan "vive la difference!" Merital 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.
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 - particularly women - 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. Marketed as Zyban, bupropion is good for giving up smoking. Scandalously, bupropion isn't licensed and marketed as an antidepressant in Europe - though doctors may prescribe Zyban
to non-smoking depressives "off-label".
Amineptine (Survector) is a clean-ish, (relatively) selective dopamine reuptake blocker. Higher doses promote dopamine release too. Amineptine is pro-sexual and 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". FDA pressure recently led to its withdrawal in Europe too. This drove it onto the pharmaceutical grey market, discomfiting doctors and patients alike.
REBOXETINE; ADRAFINIL; MODAFINIL
Reboxetine (Edronax) is a well-tolerated, selective "noradrenergic" agent. Crudely, whereas serotonin plays a vital role in mood, noradrenaline is essential to maintaining drive, vigilance and the capacity for reward. There's a fair bit of evidence that chronically
depressive people have dysfunctional and atypical noradrenergic systems - particularly their alpha2- and beta-adrenoceptors. Reboxetine itself typically doesn't have the disruptive effects on cognitive function or psychomotor performance common to older clinical mood-brighteners - though alas antimuscarinic effects are still not completely absent. The new NorAdrenaline Reuptake Inhibitors (NARIs) - and dopaminergics like amineptine (Survector) - may be especially useful in drive-deficient "anergic" states where the capacity for sustained motivation is lacking; and for melancholic depressives with a poor ability to cope with stress. Reboxetine may be safely combined with an SSRI, though there is evidence that NARIs themselves indirectly enhance central serotonin function by a mechanism that doesn't depend on reuptake inhibition. More surprisingly perhaps,
preliminary studies suggest reboxetine can actually reverse tranylcypromine-induced hypertensive crises. The "cheese effect" is triggered by ingesting tyramine-rich foods. Thus NARIs plus MAOIs may prove a potent form of combination-therapy if first
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. Alpha1-adrenergic agonists like adrafinil (Olmifon) and modafinil (Provigil) are centrally-acting psychostimulants that can brighten mood and sharpen mental focus. They stimulate the noradrenergic
post-synaptic receptors, increase glutamatergic transmission, and activate the wakefulness-promoting orexinergic neurons, thereby boosting alertness, memory 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; and in
September 2003, an advisory panel to the FDA endorsed its use for treating shift work sleep disorder and sleep apnea] 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 cheap.
MIRTAZAPINE; NEFAZODONE; VENLAFAXINE; DULOXETINE; ROLIPRAM
normally activating. Anxious and depressive insomniacs, on the other hand, may benefit more from "dual-action" mirtazapine
Mirtazapine (Remeron) is a structural analogue of the off-patent mianserin (Bolvidon). It is a comparatively new drug - a so-called NaSSA. By blocking the inhibitory presynaptic alpha2 adrenergic autoreceptors and stimulating only the 5-HT1A receptors, mirtazapine enhances noradrenaline and serotonin release while also blocking two specific (5-HT2 and 5-HT3) serotonin receptors implicated in dark moods and anxiety. By contrast, stimulation of the 5-HT2A receptors accounts for
the initial anxiety, insomnia and sexual dysfunction sometimes reported with the SSRIs; stimulation of the 5-HT3 receptors
causes nausea. Unfortunately, mirtazapine is a potent blocker of the histamine H1 receptors too. So it tends to have a somewhat sedative effect. This profile may be good for agitated depressives and insomniacs. Again, it is scarcely a recipe for life-affirmation.
Nefazodone (Serzone) is another newish, "dual action", mainly serotonergic agent. It inhibits the reuptake of serotonin while displaying
post-synaptic 5-HT2A-receptor antagonism. This may be useful for anxious depressives; but again, it may cause feelings of weakness, drowsiness
and lack of energy. Nefazodone is less likely to cause priapism than its older cousin trazodone (Desyrel). It is less likely to cause sexual dysfunction than the SSRIs. But nefazodone can also be toxic to the liver, albeit rarely. It may soon be withdrawn.
Venlafaxine (Effexor) is a phenethylamine. Thus it's a benign if distant chemical cousin of MDMA. Its manufacturers launched it as "Prozac with a punch". Venlafaxine inhibits the neuronal reuptake of serotonin, noradrenaline
and dopamine in descending order of potency. If dopaminergically augmented, it offers another opening for creative psychopharmacology. Such augmenation-therapy remains (almost) clinically unexplored. Taken on its own at low dosage, venlafaxine acts primarily as a serotonin re-uptake inhibitor. At
the high-level dosages most suitable for melancholic and hypersomnic temperaments, its noradrenergic (and weakly dopaminergic)
action becomes more pronounced. Venlafaxine lacks anticholinergic activity; but some users are troubled by its antihistamine
side-effects. Like the SSRIs, it is useful for a broad spectrum of disorders beyond clinical depression.
It is possible that duloxetine (Cymbalta), due to be FDA-licensed in 2004, and milnacipran (Ixel), available in Europe, may be more effective than venlafaxine for a segment of the population that can benefit from
dual serotonin-noradrenaline reuptake inhibition. Pain-ridden and melancholic depressives in particular may respond well to this class of drug. Once again, dopaminergic augmentation may be beneficial for the naturally lethargic. Unlike venlafaxine, duloxetine exerts its more balanced serotonin
and noradrenaline reuptake inhibition throughout the dosage range. Duloxetine also weakly inhibits the reuptake of dopamine,
and shows minimal affinity for the histamine and cholinergic muscarinic receptors. But it takes time to separate genuine therapeutic
advance from drug company hype, typically not until the patent expires.
Phosphodiesterase-inhibitors, both selective (e.g. the PDE type 4 inhibitor
rolipram) and unselective, are another under-used option. The next few decades will take us much closer to the downstream intra-cellular action. For it is here that our minds will ultimately be healed, genetically or otherwise.
is important for a different reason altogether. Many constitutionally unhappy people refuse to have anything to do with orthodox
western medicine. They won't take "unnatural" pharmaceutical
products at all. In consequence, they spend much of their lives trapped in a squalid psychochemical ghetto of chronic low
spirits. The only sort of remedy that they'll conceivably contemplate taking must carry a "natural
" label and soothingly "herbal
Unfortunately, most folk remedies are only marginally effective. Our drug-metabolising
enzymes are the product of an evolutionary arms race to counteract plant toxins. For plants tend to manufacture psychotropics because they poison or debilitate creatures tempted to eat them - not to heal our psychic woes. The Wisdom Of Nature is a
quaint piece of make-believe. Perversely, several of the natural remedies that sometimes actually work - notably Cannabis sativa, Erythroxylon coca and Papaver somniferum - are now illegal. Other "natural" options are extremely limited. But two worth exploring are SAMe and St John's wort.
Hypericum, the active ingredient in St John's wort, appears to be an effective mood-brightener and anxiolytic - by today's standards
at least. Its side-effect profile and efficacy in mild-to-moderate depression compares favourably with its synthetic counterparts. Hypericum's blend of serotonin-reuptake
inhibiting and (mild) MAO-inhibiting properties (not a combination otherwise to be explored with potent synthetics:
the risk of the potentially fatal serotonin syndrome is too great) contributes to - without wholly explaining - its generally benign effects. Once again, much more research is needed, preferably not bankrolled by the makers of lucrative competing products. Faith in the integrity of biological psychiatry would be greater if the strongest predictive factor in the outcome
of any published clinical trial wasn't the identity of the funding body.
One further remedy, albeit at "unnatural" doses, is worth noting.
levels tend to be low in depressives and high in euphoric
people. Taking myo-inositol as a food supplement in doses of 12g and more per day represents perhaps the first successful
use of the precursor
strategy for a second messenger rather than a neurotransmitter in the search for long-term mood-brightening agents. Inositol
and its derivatives serve as messenger molecules within the nervous system. The molecule itself is a naturally occurring isomer
of glucose. It is a key intermediate of the phosphatidyl-inositol cycle. This is a second-messenger system used by several
noradrenergic, serotonergic and cholinergic receptors. Adult westerners typically consume about one gram of inositol per day
in their food. The richest dietary sources are fruits, nuts, beans and grains. The mood-darkening ("stabilising") effect of
in manically euphoric people may be explicable in terms of its inositol-depleting effect. Potentially, if taken in high doses,
inositol seems to be a good way of lightening the spirits and diminishing anxiety in "euthymic" and depressed people alike.
Dosages of even 50g and more reportedly produce no toxic side-effects. This regimen shouldn't be attempted unsupervised by
people with a history of bipolar disorder
. As usual, much more research is in order. One "problem" is that naturally-occurring compounds - such as inositol and SAMe
- can't be patented. So the scope for high profit-margins is diminished. Progress is unlikely to be brisk.
THE MAO INHIBITORS
A further option involves using both some of the oldest and the newest
drugs on the block, the monoamine oxidase inhibitors (MAOIs). The older irreversible MAOIs certainly shouldn't be combined with SSRIs, and inadvisably with stimulants and many other drugs. Yet both old and new, they do have some very interesting properties.
MAOIs may be particularly useful for rejection-sensitive, so-called atypical depressives who have "reversed vegetative symptoms" i.e. overeating and oversleeping.
Monoamine oxidase has two main forms, type A
and type B
. They are coded by separate genes. MAO may be inhibited with agents that act reversibly or irreversibly; and selectively
or unselectively; these categories are not absolute. MAO type-A preferentially deaminates serotonin and noradrenaline, and
also non-selectively dopamine; type B primarily metabolises dopamine
(the "chocolate amphetamine
") and various trace amines
The substantial mood-elevating properties of the MAOIs were discovered
quite by chance in a US veterans hospital early in the 1950s. Many patients given the anti-tuberculotic drug iproniazid were not merely cured of their tuberculosis. They became exceptionally happy as well. The animated enthusiasm for life of
a previously crotchety bunch of old soldiers disconcerted their doctors. For it transpired that their new-found euphoria wasn't
just an understandable reaction to being cured of physical disease. MAOIs typically have mood-brightening properties as well.
At the time, there was no accepted and clinically effective treatment for depression. Fortunately, via the usual circuitous
routes, the appropriate lessons were eventually drawn. Many millions of people were successfully treated with MAOIs in consequence.
Sadly, the role of MAO in deaminating tyramine (from the Greek word tyros, meaning cheese) wasn't at first understood. Certain MAOI-treated patients suffered hypertensive
crises after eating varying amounts of tyramine-rich aged cheese; and several died. It is now recognised that the use of any
MAOI which is both irreversible and unselective must be accompanied by dietary restrictions. But the adverse publicity of the
initial inexplicable fatalities, combined with the introduction of a succession of dirty but sometimes tolerably effective
tricyclic compounds, sent the use and reputation of MAOIs into a precipitous decline from which they still haven't fully recovered.
The older non-selective and (more-or-less) irreversible inhibitors tranylcypromine (Parnate), phenelzine (Nardil) and isocarboxazid (Marplan) are nonetheless valuable drugs. Outside the USA, they tend to have been eclipsed by the selective and reversible
moclobemide. Similar therapeutic agents are in the pipeline. Of greater interest still are central-nervous-system-selective compounds,
notably the neuroprotective antidepressant and anti-Alzheimer's drug TV3326 (ladostigil). MAOIs that lack the peripheral effects of currently explored drugs herald an exciting new window of therapeutic opportunity.
A recent New York study showed that smokers had on average 40% less of the enzyme, monoamine oxidase type-B, in their brains than non-smokers. Levels returned to normal on their giving up smoking. Not merely is the extra dopamine in the synapses rewarding. The level of MAO-b inhibition smokers
enjoy apparently contributes to their reduced incidence of Parkinson's and Alzheimer's disease. Unfortunately they are liable to die horribly and prematurely of other diseases first.
One option which the dopamine-craving nicotine addict might wish to explore
is switching to the (relatively) selective MAO-b inhibitor selegiline, better known as l-deprenyl. Normally the brain's irreplaceable
complement of 30-40 thousand odd dopaminergic cells tends to die off at around 13% per decade in adult life. Their death diminishes the quality and intensity of experience. It also saps what
in more ontologically innocent times might have been called one's life-force. Eighty percent loss of dopamine neurons results
in Parkinson's disease, often prefigured by depression. Deprenyl has an anti-oxidant , immune-system-boosting and dopamine-cell-sparing effect. Its use boosts levels of tyrosine hydroxylase, growth hormone, superoxide dismutase and the production of key interleukins. Deprenyl offers protection against DNA damage and oxidative stress by hydroxyl and peroxyl radical trapping; and against
excitotoxic damage from glutamate.
Whatever the full explanation, deprenyl-driven MAOI-users, unlike cigarette
smokers, are likely to be around to enjoy its distinctive benefits for a long time to come, possibly longer than their drug-na´ve
contemporaries. For in low doses, deprenyl enhances life-expectancy, of rats at least, by 20% and more. It enhances drive, libido and motivation; sharpens cognitive performance both subjectively and on a range of objective tests; serves as a useful adjunct
in the palliative treatment of Alzheimer's and Parkinson's disease; and makes you feel good too. It is used successfully to treat canine cognitive dysfunction syndrome (CDS) in dogs. At dosages of around 10 mg or below daily, deprenyl retains its selectivity for the type-B MAO iso-enzyme. At MAO-B-selective dosages, deprenyl doesn't
provoke the "cheese-effect"; tyramine is also broken down by MAO type-A. Deprenyl isn't addictive, which probably reflects
its different delivery-mechanism and delayed reward compared to inhaled tobacco smoke. Whether the Government would welcome
the billions of pounds of lost revenue and a swollen population of energetic non-taxpayers that a switch in people's MAOI
habits might entail is unclear.
Untike deprenyl, the novel irreversible
selective MAO-B-inhibitor rasagiline
(Agilect) is not metabolized to methamphetamine or amphetamine. These trace amines are unlikely to contribute to deprenyl's
action. Barring unexpected delays, rasagiline is expected to gain a product license in late 2004 for the symptomatic treatment
of Parkinson's disease
. Long-term clinical trials of their comparative efficacy and safety are needed.
Humans now have the capacity to choose their own individual level of activity or inhibition of the two primary
monoamine oxidases. This does not quite enable the fine-tuning of personality variables with the functional equivalent of a graphic equaliser.
It still represents a promising start. In MAO-inhibition, as in life, more is not always better. Excessive dosages of l-deprenyl,
for instance, may actually shorten, not increase, life expectancy - at least in Parkinsonians if it's combined with
l-dopa. And levels of above 80% inhibition of MAO-A may lead to a sharp and possibly unwanted fall in dopamine synthesis. Repairing Nature's niggardliness will be a priority for the decades ahead.
Moclobemide (Manerix, Aurorix), the "gentle MAOI", is both a selective
and reversible inhibitor of MAO-A. It marks the first RIMA to win clinical acceptance. It lacks anti-cholinergic side-effects. No dietary restrictions are needed. It is valuable as
more than a mood-enhancer and resilience-booster. For moclobemide is often useful in overcoming social phobia, panic disorder, obsessive-compulsive symptoms, irritability and aggression owing to the way it enhances serotonin function. (The casual use of gobbledygook such
as "enhanced x function" will rightly alert the reader that many complications are being skirted or omitted. Those hungry
for the greater technical detail of a non-popular account can rest assured the literature will leave them feeling abundantly well-nourished).
Gentleness doesn't suit everyone. Moclobemide isn't much good at lifting deep melancholy. Tranylcypromine (Parnate), on the other hand, is one of the older and non-selective MAOIs - and is often none the worse for it. Structurally
related to amphetamine, it's generally the most stimulating, dopaminergic and relatively fast-acting of the MAOIs. Some doctors are uncomfortable with its properties. This isn't just
because of the dietary restrictions it demands. In adequate doses, it tends to induce a mild euphoria even in "normal" subjects.
In fact, its nicest effects, as for all of the compounds cited here, will vary in nature and extent from person to person.
To some extent, optimal dosage and long-term drug-regimen of choice can be discovered only by cautious empirical investigation.
Tranylcypromine is of course vastly preferable to the amphetamines and cocaine. Yet frequently and perversely, the more hazardous the drug, then the easier it is to get hold of in our society. The carcinogenic
cocktail that carries off more people than all other toxins combined can be purchased quite legally and effortlessly at any
tobacconist or newsagent. Obtaining the less lethal - but scarcely desirable - street opioids and psychostimulants requires a little more exertion. Yet they can still be readily purchased in pubs and clubs in all the big towns and cities.
Many of the more beneficent drugs discussed here, on the other hand, are unlicensed, "investigational", or available on a
prescription-only basis. They're not illegal to possess. But they are hard to obtain short of visiting countries where they're
available over-the-counter or paying high mail-order prices for an uncertain service.
If the central principle at stake here were the preservation of a drug-free
society, then some sort of totalitarian (or, more euphemistically, paternalistic) argument could be cobbled together for violating
personal freedom so oppressively. Yet that's rarely the issue. For in most cases, the issue effectively amounts, not to drugs
or no drugs, but to allowing people the choice to opt for better ones. Perhaps 80% of the population in Western countries
currently drink alcohol or smoke cigarettes. Often they do both. Whether viewed in terms of mortality, morbidity or overall quality of life, we'd be better off if we
switched to enhancing receptor sub-type selective dopaminergic, opioidergic, serotonergic and cholinergic function by the relatively
safe and crude agents touched on here; and perhaps to the more exciting products under development. As a basic minimum, people shouldn't be legally robbed of the right to do so.
This freedom of choice isn't conventional wisdom. It will be suggested
that the level of medical expertise required to make informed choices exceeds that of the average layperson; and a quasi-priestly
caste wielding the power of the prescription-pad would doubtless wish to keep it that way. But the intrinsic difficulty and
complexity of psychopharmacology or nutritional medicine, say, doesn't demand greater mental effort than, for instance, all those thousands of grimly unnatural hours spent by school
students learning mathematics. Moreover it's far more interesting to study something palpably relevant to one's emotional
well-being than something that demonstrably isn't. The notion of an education system geared to schooling people in, and for,
happiness would nonetheless strike adherents of the reigning educational orthodoxy as abhorrent were it not so largely incomprehensible.
WORKING FOR A DRUG-FREE FUTURE
Suppose, for a moment, that the reproductive success of our DNA had been best served by coding for ecstatically happy vehicles
rather than malaise-haunted emotional slum-dwellers. If this had been the case, then none of the pharmacological interventions
discussed in The Good Drug Guide would be necessary. Life-long well-being would seem only "natural". We would all enjoy
gloriously fulfilled lives. Each day would be animated by gradients of bliss. Unpleasant states of mind would be viewed as a tragic aberration. They'd be diagnosed as a freakish but clinically treatable
type of psychopathology.
Of course, it didn't work out that way. Instead, the inclusive fitness of our genes has been promoted by the "natural" manufacture of some of the most vicious psychological adaptations imaginable.
The rot goes deeper. Selfish DNA can count on innumerable dupes to act as its distal representatives even today. The need for "character-building" emotional
pain gets justified with all manner of sophistries, both religious and profane. Suffering is good for you, one may be told.
It's all part of life's rich tapestry.
It exists because it was good for our genes. Apologists for mental pain are serving as the innocent mouthpieces of the nasty bits of code which spawned them. If pressed,
DNA's unwitting spokesmen would presumably disavow the connection. Yet if one were purposely building an intelligent
robotic survival-machine, then endowing it with the illusion of free-will would prove a highly fitness-enhancing adaptation.
It's a trick which our genes merely stumbled upon; and then blindly exploited.
Fortunately, within the next few centuries humanity will be able to outwit
its ancient genetic masters. Our present status as throwaway genetic vehicles will finally be subverted. When heavenly well-being becomes the genetically
predestined norm of mental health, then the very notion of tampering with our new-won "natural" condition and feeling "drugged" will
come to seem immoral. It will also seem perverse. Why should anyone want to contaminate the divine ecstasy of their spirituo-biological
soul-stuff with chemical pollutants? No thanks.
Today's twisted victims of the primordial genetic code, on the other hand,
view the notion of sullying their natural state of being through drugs with a much more deep-seated ambivalence. They adopt it as a near-universal practice. Given
the inadequacy of the third-rate stopgaps on offer, and the lack of serious drug-education, it's scarcely surprising we're
so poor at using them. Thus concerned parents are surely right to worry about the trashy street drugs taken by their kids.
Yet with the right new genes and designer-drugs, there's no reason why mature Post-Darwinian life shouldn't just get better and better.