Once we can map comprehensively all the characteristics of the prevailing mental illnesses, the reasoning goes, we should then be better equipped to treat them appropriately.<\/p>\n
According to Hannah Ritchie and Max Roser<\/a> of Our World in Data, more than one in ten people on Earth are walking around with a mental health issue. And the World Health Organization<\/a> (WHO) insists that \u201cOne in four people in the world will be affected by mental or neurological disorders at some point in their lives.\u201d<\/p>\n To get a handle on our prolific mental unruliness, a slew of experts goes through a painstaking effort to classify all the different psychiatric conditions. It turns out that there is a whole plethora of them.<\/p>\n The North America\u2019s leading guide, i.e. the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), comes up with an encyclopaedic variety of no less than 152<\/a> psychiatric maladies. Admittingly, that number might be higher<\/a> still. The WHO has crafted their own catalogue. Chapter V<\/a> of their International Statistical Classification of Diseases and Related Health Problems, Tenth Edition (ICD-10), produces a staggering figure of over 300<\/a> mental and behavioural ailments. The latest version, i.e. ICD-11<\/a>, will come into force in 2022. Besides these two landmark handbooks, there are also other taxonomic systems in place, e.g. the Chinese Classification of Mental Disorders<\/a> and the Psychodynamic Diagnostic Manual<\/a>.<\/p>\n Fig. 1. The International Statistical Classification of Diseases and Related Health Problems, Eleventh Edition (ICD-11), The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), the Chinese Classification of Mental Disorders and the Psychodynamic Diagnostic Manual. (Source: American Psychiatric Association<\/a>, eatingdisordersreview.com<\/a>, tspsy.com<\/a> and guilford.com<\/a>).<\/p><\/div> In an attempt to see the forest for the trees in this maze of mental lawlessness, DSM-5 installs 20 categories<\/a> based on the distinctive features of various psychiatric disorders, whereas Chapter V of ICD-10 distinguishes 11<\/a> of them. The chapter on mental, behavioural and neurodevelopmental disorders of version ICD-11 has been modified to match DSM-5, in that it equally contains 20<\/a> main categories.<\/p>\n It is not my purpose to list and discuss all the present classes and types. Yet, what I do wish to mention is that globally the most prevalent<\/a> conditions include anxiety (284 million people as of 2017), depression (264 million), bipolarity (46 million), schizophrenia (20 million) and eating disorders (16 million).<\/p>\n Let us as an example put schizophrenia under our investigative microscope to understand in greater detail how psychiatric medication actually works.<\/p>\n In popular terms, schizophrenia is often wrongly described as having multiple personalities, which is rather an identifying mark of the dissociative identity disorder<\/a>.<\/p>\n Schizophrenia, however, is a severe and chronic mental health condition, frequently defined as a form of psychosis<\/a>, of which both hallucinations and delusions are idiosyncratic traits. The former symptom refers to the event in which we see, hear or feel things that are supposedly not real. The latter delineates an attitude whereby we rigidly cling to a particular viewpoint despite existing proof that suggests otherwise. Together with disorganized behaviour and dysfunctional thinking, these four symptoms are generally denoted as positive symptoms<\/a>, as their presence is what typifies this psychiatric malady.<\/p>\n Additional typical characteristics<\/a> that can crop up are feeling disconnected from self, lack of joy or motivation, irregular sleep pattern, self-neglect, social withdrawal and dissonance between body language and experienced emotion. These behavioural impairments are commonly called negative symptoms<\/a>, since they represent a lack of certain kinds of behaviour.<\/p>\n A troubling consequence of this illness is an impoverished life expectancy. Thomas Laursen et al.<\/a> proclaim that affected people lose approximately twenty years of their lives relative to the general population. The underlying reasons, they argue, extend to poor physical health and health care, secondary effects of antipsychotic medicines, lifestyle qualities, suicide and accelerated aging.<\/p>\n Furthermore, there is most likely a gender discrepancy in schizophrenia. For instance, Heinz H\u00e4fner<\/a> contends that \u201cthe disorder becomes manifest clearly later in women than in men.\u201d Also, he reports that oestrogen has a protective effect concerning the severity of the expressed symptoms. As a result, men would be more severely symptomatic than women at a younger age. Nevertheless, this protective effect diminishes with a progressively stronger genetic liability. And with respect to social behaviour, men would engage with a higher frequency in several detrimental styles of conduct, such as self-neglect and social withdrawal, compared to women.<\/p>\n Up to now, researchers have not yet pinpointed the primary cause of schizophrenia. The disorder is largely believed to stem from a dizzying amalgamation<\/a> of genetic, biological, psychosocial, cultural, political and other environmental influences. What is more, its emergence is closely connected to stressful life-changing events<\/a>.<\/p>\n When it comes to the choice of recovery strategy, antipsychotics usually make up the cornerstone of any proposed pathway towards betterment. Indeed, Subin Park et al.<\/a>, for example, claim that \u201cthe best available treatments appear to be antipsychotic medications (which is the first-line treatment) along with psychological and psychosocial treatments.\u201d<\/p>\n Nonetheless, it remains fact that many individuals do not have access to either proper health care or the required medicines. The WHO pertinently remarks that lack of access<\/a> to medical support helps to clarify why 90% of the cases of untreated schizophrenia are flagged in low- and middle-income countries.<\/p>\n Now that we have built up a fuller picture of what schizophrenia entails, let us next delve into the question why medication is more often than not the linchpin of its treatment program.<\/p>\n Proponents of antipsychotic drugs say taking them is essential because schizophrenia is primarily a brain disease.<\/p>\n One of them is John Gilmore<\/a> from the University of North Carolina. He puts forward that \u201cSchizophrenia is increasingly considered a subtle neurodevelopmental disorder of brain connectivity, of how the functional circuits in our brains are wired.\u201d Similarly, researchers Michael Owen et al.<\/a> affirm that this psychiatric condition \u201cseems to originate from disruption of brain development caused by genetic or environmental factors, or both.\u201d<\/p>\n Vivian Hook et al. at the University of California San Diego made further headway by identifying substantial neurochemical imbalances in schizophrenic people. What this means is that \u201cthe neurons derived from schizophrenia patients secreted significantly greater amounts of the catecholamine neurotransmitters dopamine, norepinephrine and epinephrine.\u201d, a related press release<\/a> explains. To be clear, a neurotransmitter<\/a> is a molecule discharged by neurons that enables impulses\u200a\u2014\u200ainformation\u200a\u2014\u200ato travel between neurons in our brain.<\/p>\n And some scientists have even submitted the claim that, in relation to schizophrenia, the brain structure itself is markedly different. As a case in point, Elena Antonova et al.<\/a> from King\u2019s College London assert that \u201cAlmost every cortical and sub-cortical brain structure has been found to be abnormal in schizophrenia.\u201d Moreover, recent research by Katja Koelkebeck et al.<\/a> insinuates that schizophrenic people have a lesser amount of grey matter, which impacts memory, information-processing, muscle control, speech, emotions and self-control.<\/p>\n Let us now descend to the molecular level to see what reaction current medication aims to achieve. As a case study, we will look at one of the most popular drugs to treat schizophrenia, i.e. Seroquel<\/a> or, by its generic name, quetiapine, which is a second-generation or atypical antipsychotic<\/a>.<\/p>\n Along the membrane of a neuron, we come across chemical structures known as receptor proteins. They interact with numerous incoming signals, e.g. neurotransmitters, hormones, toxins, proteins and pharmaceutical medication, depending on the type of receptor. Antipsychotic drugs are able to do their work, since their molecules attach<\/a> to the binding site of specific receptors that offset one or more symptoms of the respective mental disorder.<\/p>\n Mind you, in spite of its global popularity, the exact underlying mechanism of action of quetiapine remains, until today, poorly understood (see, for example, Sean Kim et al. (2017)<\/a>, Yusuke Morata et al. (2019)<\/a> and Amanda Silva de Miranda et al. (2020)<\/a>).<\/p>\n What we do know is that, with its chemical formula C\u2082\u2081H\u2082\u2085N\u2083O\u2082S, quetiapine<\/a> blocks several receptors simultaneously: dopamine, serotonin, adrenergic receptors and histamine. Overall, the molecular compound exhibits a calming and sedative effect, but it does not seem to fertilize addictive behaviour<\/a>.<\/p>\n Fig. 2. The molecular structure in 3D of quetiapine (Seroquel) with carbon (C; grey), hydrogen (H; white), nitrogen (N; blue), oxygen (O; red) and sulphur (S; yellow) molecules. (Source: Pubchem<\/a>).<\/p><\/div><\/figure>\n As a neurotransmitter in the brain, dopamine<\/a> or 3,4-dihydroxyphenethylamine (DA) holds sway over various behavioural processes, among which pleasure, decision-making, our way of thinking, motivation and reward. In schizophrenic brains, an excessive release of dopamine stimulates thoughts and signal networking, thereupon propagating hallucinations and delusions. Quetiapine quenches this overactive electrochemical flow, thereby dampening<\/a> the positive symptoms.<\/p>\n As a hormone and a neurotransmitter, serotonin<\/a> or 5-hydroxytryptamine (5-HT) is tasked to help regulate our mood, feelings of happiness, anxiety, states of consciousness, sleep cycles, memory, digestion and sexual desire. It steers the workings both within our central nervous system and gastrointestinal tract. By hindering the serotonin neurotransmitter receptors in schizophrenic patients, quetiapine soothes<\/a> the serotonergic overdrive in their brain. Subsequently, they feel more motivated to be social and better function in general. In other words, blocking the serotonin receptor alleviates<\/a> the negative symptoms of schizophrenia.<\/p>\n Adrenergic receptors attract catecholamines<\/a>, which are a type of neurotransmitter that prepare the body for a fight-or-flight response. These neurotransmitters, including norepinephrine<\/a> (noradrenaline) and epinephrine<\/a> (adrenaline), trigger the sympathetic nervous system, which translates, among other things, into an increased heart rate and a higher blood pressure. As we have seen earlier, schizophrenic patients possess a greater number of these catecholamines. Therefore, quetiapine blocks<\/a> these adrenergic receptors so that it reverses those health hazards.<\/p>\n In the brain, the biochemical compound histamine<\/a> acts as a neurotransmitter. When binding with histamine receptors<\/a>, these molecules govern crucial functions<\/a>\u200a\u2014\u200aenergy balance, homeostatic processes<\/a>, cognition, control of food intake and arousal. Schizophrenia tends to go hand in hand with elevated histamine levels in the cerebrospinal fluid<\/a>, which is why quetiapine is designed to obstruct<\/a> the histamine receptors.<\/p>\n Fig. 3. A schematic overview of how antipsychotic medication\u200a\u2014\u200aneuroleptics\u200a\u2014\u200ablocks dopamine at its receptors. (Source: dreamstime.com<\/a>).<\/p><\/div><\/figure>\n Many researchers call attention to the beneficial characteristics of quetiapine for the treatment of schizophrenia. Huafang Li et al. (2018)<\/a> ascertain that the antipsychotic is \u201cgenerally safe and well tolerated\u201d; Hua-ning Wang et al. (2016)<\/a> underscore that the drug \u201cameliorated the schizophrenia-like behaviors\u201d in their research trials; Jianjie Huang et al. (2019)<\/a> highlight that \u201cQuetiapine may offer an optimal benefit-risk balance when a prolactin-sparing antipsychotic is indicated.\u201d; and Zahiruddin Othman et al. (2016)<\/a> emphasize that \u201cQuetiapine is an interesting treatment option for patients at high risk for schizophrenia with prominent anxiety and\/or depressive symptoms.\u201d<\/p>\n As per the types of symptoms in schizophrenia, research conveys that, on the whole, antipsychotic medication is more successful in reducing positive symptoms than countering negative ones. Gary Remington et al.<\/a>, for one, conclude that \u201cthe newer antipsychotics are not superior to their conventional counterparts in the treatment of negative symptoms and [that] the effect in either case is modest.\u201d Peng Li et al.<\/a> push it further by arguing that these drugs even gravitate towards \u201cworsen[ing] negative symptoms, such as blunted affect and social withdrawal, as well as cognitive function[s].\u201d<\/p>\n With regard to the efficacy of restoring cognitive deficits, e.g. issues with task completion, concentration and memory, Indrani Poddar et al.<\/a> reminded us in 2019 that, \u201cwhile more than 20 years have been devoted to the development of new drugs to treat cognitive deficits in schizophrenia, none have been approved to date.\u201d By contrast, Jue He et al.<\/a> present more promising prospects, which hint that \u201cchronic quetiapine significantly attenuated object recognition memory impairment and hippocampal oxidative stress.\u201d<\/p>\n Yet, in other studies, the administration of antipsychotics bore symptomatically little or no results. Marcos G\u00f3mez-Revuelta<\/a> et al. documented such findings in 2018, whereby they noted that psychiatric patients \u201cwere more likely to discontinue treatment due to nonefficacy.\u201d One of the tested drugs involved was quetiapine. Such outcomes fall in line with earlier conclusions drawn by Jari Tijhonen et al.<\/a> in 2017, inferring that quetiapine is associated with a high risk of rehospitalization.<\/p>\n Notwithstanding on-going progress, ensuring effective antipsychotics is not an easy endeavour. In a recent meta-analysis conducted by John Lally and James MacCabe<\/a>, the authors remark that \u201cwe still remain a long way from being able to recommend with precision, specific treatments for individual patients, in terms of the clinical response and lack of adverse events.\u201c<\/p>\n And surely enough, quetiapine comes with important side effects<\/a>. For instance, hampering histamine receptors can prompt somnolence (extreme sleepiness), dizziness or weight gain, while barring adrenergic receptors can lead to orthostatic hypotension (low blood pressure). In addition, disabling dopamine receptors implies<\/a> an exposure to cultivating the neuroleptic malignant syndrome<\/a>.<\/p>\n Then again, a literature review by Chanoch Miodownik and Vladimir Lerner<\/a> informs us that quetiapine is found to be advantageous for the treatment of schizophrenia; that it has a relatively safe side effect profile; and that most of the reported serious events relate to overdose.<\/p>\n Fig. 4. Number of prescriptions for second-generation antipsychotics ordered by psychiatrists between 2005 and 2012 in Canada. (Source: Paper Tamara Pringsheim and David Gardner<\/a>).<\/p><\/div><\/figure>\n Whatever the final verdict will be, much uncertainty continues to exist today predominantly regarding its long-term repercussions, when all the while the United States Food and Drug Administration (FDA) approved Seroquel in 1997.<\/p>\n As a matter of fact, the FDA<\/a> openly admits that we are in the dark for what lies ahead: \u201cThe efficacy of SEROQUEL in schizophrenia was established in short-term (6-week) controlled trials of schizophrenic inpatients [\u2026]. The effectiveness of SEROQUEL in long-term use, that is, for more than 6 weeks, has not been systematically evaluated in controlled trials. Therefore, the physician who elects to use SEROQUEL for extended periods should periodically re-evaluate the long-term usefulness of the drug for the individual patient.\u201d<\/p>\n The ambiguity relative to the pharmacological consequences in the long run surrounds antipsychotics at large. Though Chen Zhang et al<\/a>. assert that \u201cthe effectiveness of different types of antipsychotic drugs is equivalent\u201d, Heidi Taipale et al.<\/a> stress the importance of the timescale, indicating that \u201cVery little is known about the comparative long-term effectiveness of novel antipsychotics.\u201d<\/p>\n This is a concern for the reason that, \u201cDue to the complexity of schizophrenia, patients need long-term medication treatments\u201d, according to Chen Zhang et al. In an apparent attempt to sound somewhat optimistic, the authors further add that, at least, \u201cthe adverse reactions of different types of antipsychotic drugs are clear.\u201d<\/p>\n Although, broadly speaking, psychiatric medication seems to make advancements in its efficacy, more research is certainly called for to provide compelling answers to the question which drugs are most accommodating, if at all.<\/p>\n Undoubtedly, many people are helped through medication, as these drugs assist them with managing their daily life. There is a segment of this medicating population, however, that is suffering unnecessarily as a result of antipsychotic medicines. In the United States (U.S.), 24%<\/a> of the population is on antipsychotics, of which roughly 30%<\/a> is supposedly worse off due to the treatment. In 2015, one study<\/a> in the United Kingdom (UK) examined people with intellectual disability. Of the 33,016 adults, 28% received antipsychotic medication, and a whopping 71% of that percentage \u201cdid not have a record of severe mental illness.\u201d<\/p>\n It speaks for itself that we cannot lump all the psychiatric maladies together and apply a one-size-fits-all mindset of \u2018to medicate or not to medicate\u2019. Nor does one or more controversial incidents decide upon the drug\u2019s ineffectiveness\u200a\u2014\u200aremember Dan Markinson<\/a> in the case of quetiapine\u200a\u2014\u200aand should it consequently be withdrawn from the market.<\/p>\n As the total effect of quetiapine externalizes differently<\/a> in every person, taking such antipsychotics remains thus a very individual decision. But precisely because of that subjective element, I find it worthy to sketch out viewpoints and practices that explore the grounds off the traditional trail.<\/p>\n Before doing so, let us take note of two interrelated, mutually reinforcing observations that could possibly lead us out of\u200a\u2014\u200aor deeper into\u200a\u2014\u200athe pharmaceutical labyrinth.<\/p>\n First off, it is not too unfair to acknowledge that the opposite side of the medical coin lies within overdiagnosis. The mixture of online information ubiquitously available to the patient and the ever more detailed description of various mental illnesses to support the physician results in a higher likelihood to take ordinary hardship, such as grief, for abnormal behaviour when, in fact, it is not. A couple of pills in a bottle after a consultation with a physician is then not too much of a stretch.<\/p>\n Secondly, we must contemplate what being labelled with a psychiatric condition does to us psychologically. It is rather unrealistic to assume that such intimate portrayal of who we are will not leave a mental imprint of some sort. In more straightforward terms, there is a hazard of self-fulfilling prophecy: the diagnosis may lead us to believe that it is the only sensible explanation for our allegedly erratic behaviour and thoughts. Hearing the actual name of the disorder pronounced by a professional psychiatrist affirms our initial suspicion that there is something wrong with us. And it now becomes all the more plausible to accept that medication is the best way forward.<\/p>\n But what if there are other explanations for the inexplicable events, which we have not yet considered?<\/p>\n The British Psychological Society (BPS), no less, writes in their report \u2018Understanding Psychosis and Schizophrenia\u2019<\/a> that \u201cHearing voices or feeling paranoid are common experiences which can often be a reaction to trauma, abuse or deprivation. Calling them symptoms of mental illness, psychosis or schizophrenia is only one way of thinking about them, with advantages and disadvantages.\u201d<\/p>\n Fig. 5. The report \u2018Understanding Psychosis and Schizophrenia\u2019 by the British Psychological Society. (Source: communityaccess.org<\/a>).<\/p><\/div><\/figure>\n In that same report, the BPA goes on to claim that psychiatric medication is merely suppressing the expressive manifestation of the malady. That is, \u201cMany people find that \u2018antipsychotic\u2019 medication helps to make the experiences less frequent, intense or distressing. However, there is no evidence that it corrects an underlying biological abnormality. Recent evidence also suggests that it carries significant risks, particularly if taken long term.\u201d<\/p>\n In some parts of the world, hearing voices or seeing (dead) people who are not physically there is interpreted as a herald of visionary personality traits. Hallucinations are envisaged as a golden ticket to a revered career as shamanic healer. What we typically call psychosis is in the shamanistic view a process of re-awakening as human being. The tradition of shamanism is celebrated among diverse cultures, including Mongols<\/a>, Sakha (Yakut)<\/a>, Tukano<\/a>, Cape Nguni<\/a>, Navajo American Indians<\/a> and Tinguians<\/a>. The documentary film \u2018Crazywise<\/a>\u2019\u200a\u2014\u200ascroll down to the end of the article and insert the password \u2018CWDUTCH\u2019 to watch the video\u200a\u2014\u200afollows two psychiatric patients on their mental journey. One of them retrieves her inner peace, away from the drugs, by embracing shamanism.<\/p>\n Inasmuch as not everyone feels or heeds the call to become a shaman, hearing voices could alternatively be linked to a greater sensitivity to spirituality. For instance, researchers Simon McCarthy-Jones et al.<\/a> determine that \u201cThe categories of psychotic and spiritual voice-hearing appear to be significantly fluid.\u201d And Philippa Richardson<\/a> fittingly remarks that \u201cAnother explanation for individual\u2019s being able to hear voices, is that of clairaudience, a psychic ability.\u201d<\/p>\n This spiritual skill holds an eye-opening, healing potential in that a \u201cClairaudient ability has a positive connotation upon the ability to hear voices, whereas the diagnosis of Schizophrenia is most commonly treated with pharmaceutical drugs to reduce or eliminate symptoms.\u201d, Richardson continues. Other voices resound such interpretations, like the one of Anna Beyer<\/a>. She ascertains that \u201cparapsychological explanations, for example understanding \u2018voices\u2019 as telepathy or spirit communication, are possible.\u201d<\/p>\n There is actually a case to make around the inclusion of spirituality within psychiatric treatment. In one research project with psychiatric residents as study subjects, Thomas McGovern et al.<\/a> observe that \u201cThere was a strong agreement (85.7%) among residents that psychiatry should not distance itself from religiousness and spirituality.\u201d Similarly, psychotherapist and university professor Vincent Starnino<\/a> points out \u201chow people with psychiatric disabilities draw upon spirituality to cope as they strive for recovery.\u201d<\/p>\n Not to mention the book \u2018Psychiatric Medication and Spirituality: An Unforeseen Relationship\u2019<\/a>, in which researcher Lynne Vanderpot addresses the positive and negative aspects of how antipsychotics intertwine with spirituality. Although Vanderpot admits that such unusual connection is hard to swallow \u201cbecause we have been so conditioned to see states of mental illness and health as fundamentally biological\u201d, she nevertheless hopes that her book \u201cexpands the conversation around psychiatric medication to include spirituality.\u201d<\/p>\n On a more practical note, Narendra Kumar Singh et al.<\/a> list a range of spiritual-minded group activities that can be embedded into psychiatric practice: \u201cspiritual autobiography, discussion of key existential issues, silent prayer and meditation, guided imagery, practice in religious rituals, use of selected readings, and attendance at religious services.\u201d In their academic paper, Alexander Moreira-Almeida et al.<\/a> equally bring forward concrete \u201cguidelines for spiritual assessment and integration thereof into mental health treatment.\u201d<\/p>\n![\"The](\"https:\/\/i0.wp.com\/cdn-images-1.medium.com\/max\/800\/1%2A-6sZHAxbYf6FqQcif8z7WA.png?resize=575%2C230&ssl=1\" "\\"The")
Unscrambling Confusing Signals<\/strong><\/h2>\n
Yes, Medication Is Necessary<\/strong><\/h2>\n
Brainy Scientists<\/strong><\/h4>\n
Inside Our\u00a0Head<\/strong><\/h4>\n
![\"The](\"https:\/\/i0.wp.com\/cdn-images-1.medium.com\/max\/800\/1%2AwpOEfce1QY16qFlr-ho7Xg.png?resize=575%2C299&ssl=1\" "\\"The")
![\"A](\"https:\/\/i0.wp.com\/cdn-images-1.medium.com\/max\/800\/1%2AparjVId_DKvpqWGmkASV9g.png?resize=574%2C439&ssl=1\" "\\"A")
Effectiveness and Side\u00a0Effects<\/strong><\/h4>\n
![\"Number](\"https:\/\/i0.wp.com\/cdn-images-1.medium.com\/max\/800\/1%2ABxtV6WxAQr8wsQQZ1OuGCQ.png?resize=576%2C413&ssl=1\" "\\"Number")
No, Thank\u00a0You<\/strong><\/h2>\n
Critical Thoughts<\/strong><\/h4>\n
Let It\u00a0Loose<\/strong><\/h4>\n
![\"The](\"https:\/\/i0.wp.com\/cdn-images-1.medium.com\/max\/600\/1%2A81ZvhgKv-fT-pQkyIGjR6A.png?resize=344%2C511&ssl=1\" "\\"The")
Spirituality in\u00a0Practice<\/strong><\/h4>\n