Psychotropic Drugs: Should I or Shouldn't I?

In developed Western countries, the tendency to place unrealistic expectations and pressures on individuals to conform to ascetic social norms that demand overuse and abuse of our mind-brain mechanisms has resulted in some very palpable but negative ramifications. The most obvious, albeit alarming, is the disarming romance afforded by the magic bullet, the perception that somebody can wave a wand and dispel psychological and physical anguish, and whatever else has temporarily disturbed our equanimity. Over and over again, doctors will reassure us that over-the-counter analgesics like Tylenol (acetaminophen) will quash the dreaded experience of pain, Valium and Librium (benzodiazepines) will reduce egregious levels of stress and anxiety, and Emadine or Livostin (antihistamines) will ameliorate eye irritations caused by allergies. There’s a magic bullet for most things, there has to be.  

By visiting a local pharmacy and perusing the shelves, one may comprehend first-hand the pharmacological armamentarium enabled by the marriage between an inherent human desire for wellness and ailment-free living, materialistic consumerism, and private pharmaceutical companies with lucrative aspirations. No doubt medical practitioners and other health care professionals with ethical sensibilities are the real losers in this affair; bombarded with subliminal messages instructing them to endorse the capitalist status quo and to appease unconscious expectations, they unwittingly introduce their psych patients to a diabolical pill-popping factory through which a deleterious cycle of distressing side effects—adaptation, habituation, dependence and addiction, iatrogenic illnesses, and premature death may be incurred.  

So much for the esteemed and sacred Hippocratic oath! I, myself, prefer to liken the supposed benefits of some psychopharmacological interventions to fool’s gold—once the novelty of the golden patina wears off, you’re left bobbing up and down like a cork in the same murky ocean that preceded your ephemeral encounter with synthetic, state-altering drugs. In other words, you’re at the foot of your problem again; back to the frightful beginning, the excruciating origin, to square one.

Prodigious medical interest in psychopharmacological agents was sparked in the early 1950s after Jean Delay, a reputed French psychiatrist, and his colleague Pierre Deniker decided to test the tolerability of chlorpromazine, known for its powerful sedative effects, on a series of psychotic patients at the Ste-Anne hospital in Paris. It was a therapeutic breakthrough of unprecedented and megalithic proportions, with clinical trials offering empirical support for chlorpromazine as an effective weapon in the long-term management of mental illness. Delay and Deniker’s publications confirmed that patients who were on the drug experienced a significant and dramatic reduction of psychotic symptoms (i.e., hallucinations and delusions), while those who decided to remain on it enjoyed fewer relapses than patients in the drug-free control group.

Since that momentous moment, psychotropic drugs have become a formidable force to be reckoned with; modern psychiatry depends heavily on them to correct the cognitive deficits and perceptual gains of atypical mind-brain states such as seen in schizophrenia, bipolar disorder, depression, and PTSD, and neurologists and other medical practitioners may deploy them to negate the neuropsychological sequelae of organic conditions like Parkinson’s, Alzheimer’s, and tumors.

Biochemical research into pharmaceuticals has opened up a brave new world, a chemical world at that; we know that their therapeutic efficacy has undoubtedly revolutionized the diagnostic aspects and prospective treatments of contemporary psychiatric medicine, but we have also ascertained that their mode of action is unspecific and for the most part problematic, leaving much to be desired. In light of such an ambivalent reality, one cannot help but feel that the problematic nature of pharmaceutical agents should be properly comprehended and their benefits and detriments appropriately weighted before we decide to accept or reject them as catalysts in the repossession of our own psychological and physical health. For that, we need to acquire, at the very least, a rudimentary understanding of how natural chemicals called neurotransmitter molecules are produced and utilized by the nervous system and how synthetic drugs interrupt these physiological control mechanisms to yield desirable modifications in the subjective experience of ‘abnormal’ states. 

Anybody with a cursory acquaintance with the clinical neurosciences will know that transfer of information in the nervous system occurs between specialized cells called neurons. Neurons themselves morphologically resemble trees and consist of a soma or cell body containing metabolic machinery; outstretched nerve branches that serve as input for incoming electrical messages called dendrites; and an axon, a single efferent projection whose purpose is to pass information to the dendrites of other neurons. In a most fascinating phenomenon, the axon terminals projecting the encoded information and the nexus of dendrites receiving it never actually make physical contact. The vacant junction is called a synapse.

Perhaps one way of understanding nerve cell linking is to evoke a direct comparison with Rodin’s marble sculpture, The Kiss, which originally embellished the epic bronze portal, The Gates of Hell— just as a statue of a forbidden couple may convey the magnetic, binding power of romantic love and eroticism without their lips touching, so too is information ferried across the synaptic junction in the complete absence of any physical apparatus. When a nerve cell is stimulated to convey an encoded message, it will discharge chemical molecules called neurotransmitters into the junction, allowing the information to hitch a chemical ride across to the postsynaptic terminal of the afferent nerve cell. Receptors embedded on the surface of its membrane act as gatekeepers and will accept or reject incoming signals. Transfiguration in the shape of the receptor means the message has been accepted and transmuted into an excitatory effect that may be conducted along the afferent neuron as an action potential; alternatively, inactivity at the receptor site translates to an inhibitory effect where the docking neurotransmitter is refused passage, kept afloat in the synaptic junction, and subsequently swallowed up by enzymes, special proteins which augment chemical reactions in our bodies.

Pharmaceutical agents enforce change at the chemical level of physiological function in one of three ways: they can closely mimic the molecular structure of a particular neurotransmitter so that the postsynaptic neuron is fooled into firing an action potential, called agonistic action; they can bind to specific receptors on postsynaptic terminals and inhibit neurotransmission, called antagonistic action; or they can operate via consolidation of the two aforementioned actions. To give an example or two, drugs with some psychotropic properties substances like heroin, methadone, and morphine are agonistic because they activate opioid receptors in the brain, naltrexone and naloxone are antagonists that block the same opioid effects by attaching to opioid receptors and inhibiting transmission, and the pharmacological taxonomy containing buprenorphine and butorphanol exhibit both agonistic and antagonistic properties.

Now all would bode well if drugs acted naturally in their manner of operation and enforced enduring changes at the fundamental genetic level, or if there was an ingenious way of containing a particular drug in one specific area of the human body after ingestion and inoculation. Lamentably, drugs are synthetic products employing biochemical pathways of unspecific action. Concerning the latter, once the drug has entered the bloodstream it is free to circulate and go anywhere—eyes, mouth, heart, stomach, and so forth. Even that superior holocephalic fortification, a membrane known as the blood-brain barrier, cannot guarantee absolute fortification for our most delicate and vital organ, the human brain.

Recreational drugs are notorious for their ability to penetrate this defense and change brain chemistry, often with disastrous consequences. More importantly, perhaps, the principal neurotransmitters like serotonin, norepinephrine, and acetylcholine are intricately woven into a physiological control system that deploys each for the regulation of manifold cognitive, emotional, and physiological functions.

Norepinephrine, for example, is bequeathed the imperative cognitive task of attentional selectivity and concentration in the brain and the activation of the sympathetic branch of the autonomous nervous system. There is a wide gamut of functions associated with the sympathetic nervous system: the suppression of appetite and digestion, the glandular effusion of adrenaline, the inhibition of blood flow to the genitals, the augmentation of heart rate and respiration, and a lot, lot more. It would make sense then to surmise that deficits in any of these functions are intimately bound up with significant decreases in the neuronal output of norepinephrine.

Nowadays prescriptions of a mild amphetamine, a close chemical cousin of norepinephrine, are the pharmacological treatment of choice for psychiatrists attempting to reduce the disturbing motor movements of children suffering from that dreaded demon called attention deficit disorder (ADD/ADHD). In the parlance of modern psychiatric discourse, the immediate suppression of random motor signals with these drugs makes possible enhanced present-moment awareness and reduces distractibility and rumination.

I have no reservations when it comes to the absolute potency of drug treatment—the amphetamines offer satisfactory short-term relief from undesirable symptoms by artificially stimulating the same neural pathways as norepinephrine, pathways which somehow facilitate normative attentional states in healthy individuals. But the whole endeavor takes on a much more ominous guise upon closer scrutiny; amphetamines may act to correct a “cognitive deficit” deemed a nuisance in pedagogical settings, however, you can be more than certain that they will somehow disrupt any function with which its natural counterpart (norepinephrine) is chemically affiliated. With no way of localizing pharmacological action in the brain and body, we can expect multiple functions to be affected. And guess what, they are!

Clinical trials have revealed that minimal doses of amphetamine required for a therapeutic response do come with some perturbing side effects—hyperalertness, irritability, insomnia, restlessness, an irregular heart rate, atypical breathing, hypertension, erectile dysfunction in males, and whatnot. You could probably expect the same or analogous detriments to arise if norepinephrine levels skyrocketed to double and triple figures. Scarier still is that we have at our disposal only limited information about the long-term or chronic use of psychotropics like amphetamines. The aforementioned side effects explain why a conscientious, empathic, and discerning medical professional will only prescribe drugs as a last resort.

Then there’s the problem of adaptation or “downregulation.” The human body is incredibly efficient, economic, and adaptive when it comes to the modus operandi for chemical signaling. When functioning optimally, neurons will keep moderate quantities of receptor sites open for business, enabling the swift transmission of signals (or inhibition of signals) along their axons when neurotransmitters arrive from local terminals. This evolutionary innovation of chemical control ensures that all incoming messages are attended to swiftly. Having said that, possible excesses are rarely, if ever, construed as desired amenities—flood receptor sites with high concentrations of neurotransmitters or their artificial chemical cousins for protracted periods, and the former reconfigure so that the amount made available for chemical action decreases exponentially. An intrinsic capacity for learning at the cellular level is nothing short of commendable; why should a biological system expend metabolic energy in keeping innumerable receptor sites open for specific transmitters when the broadcast of pertinent signals has already been guaranteed? It seems pointless and is.

At some point in evolutionary history, Mother Nature must have cottoned onto this small glitch in our genetic makeup and acted in favor of efficiency and economy in her apropos correction of it. All the same, for many among us this constructive intercession has become a diabolical conspiracy. Just as your close circle of faithful listeners and supporters may turn a blind eye if you cry “wolf” too many times in your life, so too do your neurons desensitize to the “call” of chemical molecules when these are in perpetual effusion. When besieged by a chemical ocean, receptor sites will remain sedentary, at least until local conditions improve. The implication for us? Well, if we make the mistake of bombarding our nervous systems with the same drug repeatedly, we habituate and our tolerance to their effects–therapeutic or otherwise–decreases.

In time the cognitive, emotional, and physical benefits facilitated by sustained drug use wane like the moon. We increase the dosage to recapture the same physical relief and psychological equipoise that we’d experienced with significantly lesser amounts in former times. Before we know it the rate of popping, puffing, injecting, sniffing, guzzling, or whatever else has increased to near-seizure levels. It has become something of a knee-jerk reaction or automatism in the face of adversity. By this stage, the transient switches in conscious states caused by pharmaceuticals have robbed us of our capacity for analytical reasoning and judgment. Our minds have become enfeebled and scrambled, so much so that we’ve now deluded ourselves into believing that more of the respective chemical is the only solution to our problems. Without knowing it we’ve become addicted.

Nature’s predilections for economy and efficiency work against us in other ways too. When transmitter saturation at any particular synapse is continuous, the efferent nerve cells will cease producing that neurotransmitter completely. From an evolutionary perspective, the conservative decision to abort seems sensible; why should the body expend energy making a product that isn’t needed? Probing a little deeper we see that this, too, poses a very significant problem for addicted individuals trying hard to abstain from drug use, or individuals being weaned off prescription drugs. It takes the neurons responsible for transmitter output an indeterminate period (days, weeks, months, etc.) to recommence production if executive commands coming from the Central Nervous System (CNS) spontaneously overturn the original decision.

A temporary lag in the production of the transmitter leaves the afferent networks shrieking and bellowing for excitation, a phenomenon that manifests on the psychological level as withdrawal. Anybody suffering from withdrawal will find that symptoms are relative to chemical quantity—the greater the prescribed dose, the more severe the withdrawal symptoms. The only escape and reprieve, at least in the short term, is to spray afferent neural networks starving for the chemical transmitter with an artificial stand-in, a drug that will act upon the same receptor sites.

For a great many the instantaneous relief offered by recourse to drugs becomes too great a temptation to resist and they capitulate, becoming nonconscious accomplices in the anomalous alteration of dynamic metabolic processes which buttress their natural biorhythms. And for disturbing these natural biorhythms our bodies will impose the most horrendous punishment—they will thrust us into a wild chronological vortex, and, deprived of all our willpower, we shall find ourselves plummeting down to the realms of tolerance and habituation, lower still to the realms of dependence, addiction, and withdrawal, and, if we’re immensely unlucky, lower still to the ravages of overdose and premature death. It would therefore be wise if we pondered the consequences of this self-perpetuating and deleterious cycle before invoking it in our lives.

In our brave new world, psychiatrists, psychiatric nurse practitioners, and many other medical professionals deploy the same pharmaceutical agents in treating individuals, who, by their idiosyncratic symptom cluster, fall into one or another taxonomic class on the innumerable list of disorders outlined in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V). According to classification system outlined in the pages of this manual, a savvy businesswoman with a grossly incapacitating and crippling level of anxiety might be treated with anxiolytics like Diazepam and Librium [SSRIs are actually first line pharmacotherapy for anxiety]; an unemployed youth of lower middle class standing who is isolating and engaged in cutting behaviors may be prescribed antidepressants of the serotonin-norepinephrine reuptake inhibitor class like Effexor and Prozac, or the tricyclic drug imipramine; a middle-aged artist trapped between ebullient mania and the inertia of depression, may be diagnosed with bipolar I disorder and given mood-stabilizers like lithium carbonate or sodium valproate; and the introverted sophomore whose mind-space is colored by incoherent thoughts and plagued by hallucinations and paranoid delusions will more than likely be diagnosed with a schizospectrum disorder and prescribed phenothiazine-derived neuroleptics like  chlorpromazine or atypical antipsychotics like clozapine and risperidone. Incidentally. there is something for every “type” of mental disturbance.  

Prescription rates have soared in the last few decades, and the zealous overprescription of psychotropic medications is a cause for concern.  In the June 2014 edition of Australia’s leading independent medical publication, Australian Doctor, writer Kate Aubusson reported that children diagnosed with autism, schizophrenia, or bipolar mania were immediately prescribed atypical neuroleptics. What is more, it appears prescription rates for psychotropics increased by a startling fifty-four percent between 2008 and 2011, with about 110 children receiving prescriptions for atypical neuroleptics in 2012.[1] When it came to prescriptions of antipsychotics for patients under nineteen years of age, an analysis of data gathered from pharmacy claims pinpointed pediatricians as the principal offenders, followed closely by GPs and psychiatrists.[2]

If this doesn’t stir feelings of disquiet and concern in community health, then I’m not sure what will. Speaking about the matter at hand, child psychiatrist Dr. Robert Adler articulates the collective concern: “I do not believe risperidone should be prescribed to under five-year-olds by a GP without specialist input,” he says. “It’s a drug with significant side effects and I would be very, very hesitant to start a child so young on such a medication.”[3]

When it comes to the long-term management of symptoms and with treatment efficacy varying from patient to patient, one would assume that the best position any informed healthcare professional should advocate for and adopt concerning prescriptive psychopharmacology is that of a conservative chemist–lowest doses for therapeutic effect, close observation and titration, and tapering off when they are no longer necessary.  

In their plight to maximize capital, pharmaceutical companies will conveniently omit or downplay the notion that iatrogenic disorders are spawned each time a prescription of neuroleptics, for instance, is handed to a patient suffering from a psychotic illness. Ever since their inception in the 1950s, conventional neuroleptics [antipsychotics] have gained international notoriety for the bizarre gamut of extrapyramidal side effects they’re known to generate, most notably akathisia, a syndrome characterized by atypical feelings of restlessness and agitation; neuroleptic dysphoria or sustained depression; uncontrollable Parkinson-like tremors; weight gain; sexual dysfunction; neuroleptic-induced deficit syndrome, a condition whereby the patient undergoes a sudden loss of motivation leading to the fulfillment of fewer life goals; and spasmodic movements of the jaw and tongue, otherwise known as tardive dyskinesia.

Doctors are frequently faced with far more insidious side effects also—serious conditions like agranulocytosis, an acute condition characterized by a significant reduction of neutrophils, a type of white blood cell produced by the immune system; a psychophysical condition combining atypical fluctuations in conscious states, fever, and muscular rigidity called neuroleptic malignant syndrome; and sudden heart failure. Ironically, many of these insidious side effects were first observed in conjunction with the desirable antipsychotic action.

Chemists wishing to dampen the extrapyramidal effects of typical neuroleptics (i.e., chlorpromazine) later developed a second generation of psychopharmaceuticals, the atypical neuroleptics (i.e., quetiapine, olanzapine, and risperidone) which were allegedly better tolerated and user-friendly. After undergoing clinical trials, it became apparent that these, too, were associated with adverse complications like hyperlipidemia, weight gain, and an increased risk for stroke and myocardial infarction.

Then there’s calamitous epiphenomena intimately bound up with but frequently perceived as independently of these side effects, such as quality of life. Side effects may become so intolerable and insufferable as to elicit suicidal ideation and worse still, suicidal attempts. Once again, the Hippocratic Oath has been obviated! In the final analysis, the synthesis and circulation of subsequent drug classes designed to eschew detrimental side effects and risks associated with a first or inaugural class of psychotropic drugs are usually no more efficacious than these and engender a different set of side effects–there is no dramatic quantifiable improvement in terms of therapeutic efficacy.  

The placebo effect, as Sybo Schouten points out, has been shown to possess 55-60 percent of the therapeutic efficacy of psychotropic medications in treating depression and alleviating pain.[4] Statistical support for an authentic and hierarchical connection between the higher faculties of cognition, emotion, and the body in maintaining homeostasis and equilibrium deserves the undivided attention of those healthcare professionals genuinely interested in integrative care and in satisfying the multilevel needs of their patients. To be sure a discerning and just clinician should be able to offer patients something more than just “band-aid” pharmacotherapy that numbs their psychological distress but doesn’t transpose or mitigate factors that actively created circumstances perceived as hostile and suboptimal. Perhaps the task of recalibration, rebalancing, and of reattuning an ailing individual to the fundamental harmony of the universe should fall squarely upon the shoulders of the mind-manipulators, or at the very least, a confluence of complimenting psychological and pharmacological/somatic interventions instead of petitioning only a cocktail of artificial exogenous chemicals to do similar, if not the same, work.  

[1] Kate Aubusson (2014), ‘Toddlers on Antipsychotics: Review Raises Concern over Soaring Prescribing Rates’, in Australian Doctor, 13 June, pp. 1-2.

[2] Ibid, p. 2.

[3] Ibid, p. 2.

[4] Pamela Rae Health, Mind-Matter Interaction: A Review of Historical Reports, Theory, and Research (Jefferson, North Carolina: McFarland & Company, 2011), p. 108.