As the schizophrenia/psychosis recovery research continues to emerge, we discover increasing evidence that psychosis is not caused by a disease of the brain, but perhaps may best be described as a last ditch strategy of a desperate psyche to transcend an intolerable situation or dilemma. To better understand how this understanding which is so contrary to the widespread understanding of psychosis has emerged, it will help if we break this discussion into two parts: (1) a summary of the research associated with the “brain disease theory” of schizophrenia/psychosis; and (2) a summary of the research that has given rise to this alternative understanding.
Part One: Taking a Closer Look at the Brain Disease Theory
In spite of over a hundred years of research and many billions of dollars spent, we still have no clear evidence that schizophrenia and other related psychotic disorders are the result of a diseased brain. Considering the famous PET scan and MRI scan images of “schizophrenic” brains and the regular press releases of the latest discoveries of one particular abnormal brain feature or another, this statement is likely to come as a surprise to some, and disregarded as absurdity by others. And yet, anyone who takes a close look at the actual research will simply not be able to honestly say otherwise. And not only does the brain disease theory remain unsubstantiated, it has been directly countered by very robust findings within the recovery research, it has demonstrated itself to be particularly harmful to those so diagnosed (often leading to a self-fulfilling prophecy), and it is highly profitable to the pharmaceutical and psychiatric industries (which likely plays a major role in why it has remained so deeply entrenched in society for so many years, in spite of our inability to validate it).
Deconstructing the Myths of Madness
The claim I am making here clearly runs counter to the mainstream understanding of schizophrenia, but we find that it’s a relatively straightforward task to back up this claim. We simply need to take the time to extract the actual research findings from the unsubstantiated assumptions and propaganda that are so often used to back up the brain disease theory. I’ll go through the most prevalent of these here:
Hypothesis #1: Schizophrenia is caused by a biochemical imbalance within the brain
This theory originated from the observation that drugs which block the transmission of the neurotransmitter dopamine within the brain (so called “antipsychotics,” originally referred to as “major tranquilizers”) appear to reduce the symptoms of schizophrenia. The reasoning behind the origin of this hypothesis was, since schizophrenic symptoms are reduced when dopamine transmission is suppressed, then perhaps schizophrenia is caused by excessive dopamine within the brain.
This hypothesis originally appeared quite plausible; however, it has since been seriously discredited:
First, although it is known that an individual’s dopamine receptors (the type of receptors most affected by antipsychotic drugs) are completely blocked within hours of consuming a sufficient dose of an antipsychotic drug, the actual antipsychotic effects often do not become apparent for up to several weeks (although a significant degree of apathy towards one’s psychotic experiences often does kick in quickly, as would be expected with any kind of tranquilizer; Bentall, 2004). If psychotic symptoms are the direct result of too much dopamine, then why don’t we see a more immediate abatement of these symptoms as soon as the dopamine levels have been effectively reduced?
Second, with the introduction of PET and MRI scans, the dopamine hypothesis was apparently substantiated when it was recognized that many “schizophrenic” brains do indeed seem to be set up to transmit excessive dopamine. However, it was eventually realized that the vast majority of brains studied had been exposed to long-term antipsychotic drugs, and it’s since been established that the effects of these drugs alone may very well account for these anomalies (Burt, Creese, & Snyder, 1977; Kornhuber et al., 1989; Mackay, 1982).
Finally, even many of the proponents of this theory have been forced to acknowledge that we still have not found any clear biochemical imbalance that we can associate consistently with schizophrenia or any of the “mental illness” diagnoses, and that all we can really say for sure is that psychiatric drugs themselves do lead to the development of a biochemical imbalance in one’s brain (Hyman & Nestler, 1996; Whitaker, 2002).
Hypothesis #2: Schizophrenia is caused by anomalous brain structures
This hypothesis essentially states that schizophrenia is a disease caused by something wrong with the actual structure of one’s brain, specifically with regard to the relative size of the cerebral cortex and/or other nearby regions of the brain. This hypothesis is generally supported by the actual findings of such anomalies of the brains of those so diagnosed. But again, upon closer inspection of the research, we find an empty hypothesis that quickly crumbles away:
First, we have discovered that there are many different factors that can lead to these abnormalities, including: depression, alcoholism, early childhood trauma (Read, 2004), water retention, pregnancy (Woodruff & Lewis, 1996), advancing age, variations in educational achievement, social class, ethnicity, and head size (Bentall, 2004). It was also discovered that the sizes of these regions of the brain can fluctuate quite rapidly within even healthy individuals, leading to varying results even within the same individual (Bentall, 2004). And once again, what do you imagine we have found that is probably the most relevant factor causing such anomalies in the brain? You guessed it… the use of antipsychotic drugs themselves. And virtually all of the research that has discovered such brain anomalies in those diagnosed with schizophrenia did not account for this very important factor, meaning that once again, most of the brains studied had most likely been adversely affected by the long-term use of antipsychotic drugs (Read, 2004; Siebert, 1999).
A second serious challenge to the validity of the abnormal brain structure hypothesis came when it was recognized that the majority of those diagnosed with schizophrenia do not show any obvious brain abnormality at all. Lewine found that “there is no brain abnormality in schizophrenia that characterizes more than 20-33% of any given sample. The brains of the majority of individuals with schizophrenia are normal as far as researchers can tell at present [emphasis added]” (Lewine, 1998, p. 499); and this in spite of the fact that most of these participants were likely exposed to other brain changing factors such as trauma and/or antipsychotic medications. Conversely, it is common to find healthy individuals who have no schizophrenic symptoms at all and yet have brain abnormalities similar to those sometimes found in schizophrenics (Siebert, 1999).
Hypothesis #3: Schizophrenia is a Genetic Disorder
This hypothesis is in close alignment with the two brain disease hypotheses mentioned above and suggests that this brain disease is transmitted genetically. But again we find some serious problems with the assumptions that have given rise to this hypothesis:
This hypothesis is based on a small handful of twin and adoption studies (Joseph, 2004) conducted many decades ago which, even when we ignore the many serious methodological flaws with these studies, the only conclusion that can actually be drawn from them is that there may be a hereditary component in one’s susceptibility to developing psychosis. However, this is not any different than the findings that there may be a hereditary component in intelligence, shyness, and other psychological characteristics that clearly are not indicative of any kind of physiological disease.
In other words, it’s an illogical leap to assume that a hereditary predisposition for a psychological trait or experience must imply biological disease. Yes, there does seem to be some evidence that some of us may be born with a temperament or other psychological characteristics which make us more vulnerable to experiencing psychosis at some point in our life; but no, this evidence does not lend any validity to the hypothesis that schizophrenia is a genetically transmitted biological disease.
Another important area of research discrediting the “genetic disease” hypothesis is the far more substantial research showing high correlations with environmental (non-hereditary) factors and the development of psychosis/schizophrenia. For example, One study looked at 524 child guidance clinic attendees over 30 years and discovered that 35% of those later diagnosed with schizophrenia had been removed from their homes due to neglect, a percentage twice as high as that for any other diagnostic category (Robins, 1974); another study found that 46% of women hospitalized for psychosis had been victims of incest (Beck & van der Kolk, 1987); another study of child inpatients found that 77% of those who had been sexually abused were diagnosed psychotic compared to only 10% of those who had not been so abused (Livingston, 1987); and yet another study found that 83% of men and women who were diagnosed with schizophrenia had suffered significant childhood sexual abuse, childhood physical abuse, and/or emotional neglect (Honig, Romme, Ensink, Escher, Pennings, & de Vries, 1998). Bertram Karon, researcher and acclaimed psychosis psychotherapist, has found evidence of a high correlation between the experience of intense feelings of loneliness and terror within childhood and the later onset of schizophrenia, a finding that is clearly closely related to the findings of these other studies (Karon, 2003).
Even the strongest proponents of the brain disease hypothesis acknowledge that it has not yet been validated
The National Institute of Mental Health, on its Schizophrenia home page, proclaims confidently that “schizophrenia is a chronic, severe, and disabling brain disorder” (NIMH, 2010a, Para. 1), a statement you find on nearly every major page or publication they have put out on the topic; and yet if you spend a little more time looking through their literature, you will find that they admit that “the causes of schizophrenia are still unknown” (NIMH, 2010b, Para. 1). Similarly, the American Psychiatric Association also confidently proclaims that “schizophrenia is a chronic brain disorder” (APA, 2010, Para. 1), but then they acknowledge on the very same page that “scientists do not yet know which factors produce the illness” (APA, 2010, Para. 10), and that “the origin of schizophrenia has not been identified” (APA, 2010, Para. 1). The strong bias towards the brain disease theory is clearly evident in the literature of these and other similar organizations, and yet the message comes through loud and clear that we still do not know the cause of schizophrenia. Even the U.S. Surgeon General began his report on the etiology of schizophrenia with the words, “The cause of schizophrenia has not yet been determined” (Satcher, 1999, Para. 1). It would appear, then, that it is simply not appropriate to claim with such confidence that schizophrenia is the result of a brain disease.
If schizophrenia really is a brain disease, then how do we account for the relatively high rates of full recovery from it?
One finding within the recovery research that is extremely robust is that many people experience full and lasting recovery after having been diagnosed with schizophrenia. We see this evidence in the vast majority of the longitudinal recovery studies (See Chapter 4 in my book, Rethinking Madness, for a complete list of all major longitudinal studies), including those conducted by the National Institute of Mental Health (Harrow & Jobe, 2007; Harrow, Jobe, & Faull, 2012) and the World Health Organization (Hopper et al., 2007). There is evidence of spontaneous recovery in between 5% and 71% of cases, depending upon the country of origin and other factors, and even as high as 82% with certain psychosocial interventions (Mosher, 1999; Seikkula, Aaltonen, Alakare, Haarakangas, Keränen & Lehtinen, 2006). It is illuminating to compare the high recovery rate for schizophrenia with the recovery rate for well-established diseases of the brain such as Parkinson’s, Alzheimer’s, Hungtington’s, or Multiple Sclerosis, in which there is no well documented evidence of even a single individual making a full recovery from any of these (Siebert, 1999). Furthermore, we see evidence that many of those who have experienced full recoveries from schizophrenia and other related psychotic disorders do not just return to their pre-psychotic condition, but experience profound healing and positive growth beyond the condition that existed prior to their psychosis, again in stark contrast to the well established diseases of the brain (Williams, 2011, 2012).
The mainstream paradigm of care may actually be creating a self-fulfilling prophecy of brain disease
While we continue to have no solid evidence that schizophrenia/psychosis is the manifestation of a diseased brain, we do discover one particularly tragic irony in that our very entrenched belief in this theory and the paradigm of care that has resulted from it is actually ensuring that enormous numbers of people actually do develop brain disease (see Figure 1).
Figure 1. A vicious circle caused by the brain disease theory of schizophrenia
Isn’t it time, then, that we finally let go of the brain disease theory?
In summary, then, we find that in spite of well over a hundred years of research and billions of dollars spent, the brain disease theory remains entirely unsubstantiated; and that our persistent yet unfounded faith in this theory may very well be generally causing much more harm than benefit (or at least causing significant harm to those so diagnosed at the cost of great financial benefit to certain key players within the current mental health care establishment).
Part Two: Towards an Alternative Understanding of Schizophrenia/Psychosis
So, if schizophrenia/psychosis is not caused by a disease of the brain, then what does cause it? This is not a simple question, and it’s further complicated by the fact that there continues to be widespread controversy over whether or not the concept of “schizophrenia” as it is currently used is even a valid construct, an issue that needs to be addressed first before suggesting an alternative model for understanding schizophrenia and the other related psychotic disorders.
Moving from discrete “mental illnesses” to a continuum of experience
The debate about the validity of the concept of “schizophrenia” arises from recent research suggesting that (1) all of the various major psychotic disorders may simply be variations of one phenomenon, and (2) there may be not be distinct boundaries between psychosis itself and what we think of as sanity. The British Psychological Society (the BPS, Great Britain’s counterpart to the American Psychological Association), in its official report summarizing their understanding of “mental illness” and “psychotic experiences,” concluded that the various psychotic disorders may more appropriately be classified as variations of one phenomenon, a phenomenon that many have suggested we refer to simply as psychosis or madness.
Taking this conclusion one step further, the BPS suggested that “mental health and ‘mental illness’ . . . shade into each other and are not separate categories” (2000, p. 17). In other words, they suggest that not only are the various psychotic disorders best understood as merely representing different points along a continuum of a single phenomenon (see Figure 2), but that sanity and madness themselves are also best understood as being merely different points along a single continuum (see Figure 3). They cite evidence suggesting that psychotic experiences are merely extreme expressions of more ordinary traits found within the general population.
Figure 2. Seeing the major psychotic disorders as lying on a common continuum.
When psychotic experiences contain primarily cognitive features (so called delusions and hallucinations), a person is most likely to be diagnosed with schizophrenia; when affective instability predominates, a person is most likely to be diagnosed with bipolar disorder; and when a person experiences a significant combination of both of these, they are most likely to be diagnosed with schizoaffective disorder.
Based upon the findings of my own research and my review of the other relevant research, I’ve come to the conclusion that it can be helpful to see the “sanity/madness” continuum as being defined by essentially two factors: (1) the degree of resonance or dissonance of one’s experiences with consensus reality (where consensus reality is defined as the understanding of reality that is generally agreed upon as being the most legitimate within a given individuals’ society); and (2) for those having experiences that differ significantly from consensus reality (let’s call them anomalous experiences), the degree of distress, limitation, and/or instability that is associated with these experiences. With these two factors in mind, then, we can divide the sanity/madness continuum into four separate categories of experience, keeping in mind that these don’t represent discrete categories but merely act as place markers along a common continuum of experience; see Figure 3).
Figure 3. The “Sanity/Madness Continuum.”
By considering anomalous experiences from a continuum perspective, we arrive at some very different implications regarding how to best define such experiences and what is the best way to support those who experience them:
First, we recognize that the line between so called “sanity” and so called “madness” is somewhat arbitrary—that it’s not helpful and probably not possible to pinpoint any discrete “illnesses” along this continuum.
Second, we recognize that the problems associated with anomalous experiences are probably not due so much to the fact that they deviate from consensus reality, but rather are more likely due to the difficult relationship an individual may have with these experiences (e.g., distress caused by hearing persecutory voices or holding persecutory beliefs, along with unusual or even harmful behavior that may arise in someone’s attempts to deal with them). One implication of this is that it’s important to distinguish between those anomalous experiences that cause distress or limitation, and those that don’t. If they’re not causing any problems, then what’s the problem? Why call it psychosis? Considering these kinds of experiences to be “psychotic” or giving them a name such as “schizophrenia” or “delusional disorder” appears to be unhelpful and likely even harmful, especially if such individuals are inculcated into the unfounded belief that these are the manifestations of a diseased brain.
A second important implication of this idea is that, when these kinds of experiences do cause distress or limitation, it’s likely that the best support we can offer does not consist of trying to bring the individual’s experience back into alignment with consensus reality, but instead consists of helping them meet their needs from within the context of their own experiences. The literature is filled with research and biographical accounts supporting this idea (for example, Chadwick, Birchwood, & Trower, 1999; Romme et al, 2009).
Finally, as an individual’s experience does move further down the continuum into the realm represented by the two categories listed at the bottom of Figure 3, evidence from my own research (Williams, 2011, 2012) as well as that of other recovery research (e.g., Arieti, 1978; House, 2001; Karon & VandenBos, 1996; Laing, 1967; May, 1977; Mindell, 2008; Nixon et al, 2009, 2010; Perry, 1999) suggests that they may be entering a powerful psychological process entailing the transformation of their self and their personal paradigm at a very profound level (more on this shortly). This is the process that often gets equated with “florid psychosis” and is typically the hallmark condition that so often gets labeled as “schizophrenia” or as one of the other major psychotic disorders.
Since the term “schizophrenia” is so heavily laden with unfounded assumptions, as we’ve been discussing, I’ll simply refer to this process as “the psychotic process” or “psychosis” in order to maintain some congruence with the terminology already used within the field (while acknowledging that the term “psychosis” also comes heavily laden with problematic assumptions). After all, we can say that the condition that so often gets labeled as “schizophrenia” (or one of the other major psychotic disorders, depending upon the specific nature of the anomalous experiences) is essentially just long term psychosis.
So, what causes psychosis?
Returning, then, to the question of what causes psychosis, I’ll preface my discussion of this question hereby saying that I’ve devoted an entire book (Rethinking Madness—Williams, 2012) to a thorough exploration of this question, so unfortunately, it’s just not possible to adequately summarize and back up a thorough answer to this question within such a brief article. What I will attempt to do here, however, is to put forth the most essential concepts of this alternative understanding and hopefully encourage others to engage in fruitful discussion about this important topic.
While I don’t believe it’s a stretch to say that our attempt to validate the brain disease theory of these disorders has so far been a colossal failure, there is a very different line of research that I believe has had much more success in providing significant clues as to the cause of these vexing disorders. The line of research I’m referring to is the research that has inquired directly into the actual lived experiences of those who have personally experienced psychosis.My own recent research is particularly relevant in this regard, which includes a series of three studies inquiring deeply into the experiences of those who have experienced full and lasting recovery from long term psychosis (Williams, 2011, 2012).
I have found that the findings of this line of research have converged sharply upon a fundamental cause of these psychotic disorders that is perhaps best stated something like this: The individual we deem “schizophrenic” or “psychotic” is merely caught in a profound wrestling match with the very same core existential dilemmas with which we all must struggle. In other words, it appears likely that psychosis is not caused by a disease of the brain but is rather the manifestation of a mind deeply entangled within the fundamental dilemmas of existence.
So, what are these existential dilemmas?
The term “existential dilemma” essentially refers to the dilemmas inherent in finding ourselves in a state of existence—“Here I am, alive, conscious, and feeling. Now what?” These dilemmas, at their core, relate to our need to maintain our existence, and perhaps even more importantly, our need to create a life that is worth living—where the joys and rewards of living are strong enough to overcome the inherent pain and suffering of life and provide us with the will to go on living. Some of the most pertinent such dilemmas that have been named by various existential thinkers are: finding a balance between love/belonging and authenticity/autonomy; finding a balance between freedom and security; coming to terms with the fact that all of our decisions and actions come at some cost; coming to terms with our own impending death; and cultivating enough meaning in our lives so that we are able to rise out of bed every morning and greet each new day.
In virtually all of the research and case studies I have come across that have looked closely at the actual subjective experiences of those who have fallen into a psychotic process, we see evidence that, prior to the onset of psychosis, these individuals had found themselves in overwhelming existential dilemmas similar to those mentioned above, but to a far greater degree than that which the average person ordinarily experiences. In one of the most well-known such studies, R. D. Laing, a Scottish psychiatrist renowned for his pioneering research on schizophrenia and his clinical work with those so diagnosed, closely studied the social circumstances surrounding over 100 cases of individuals diagnosed with schizophrenia, and he concluded that “without exception the experience and behavior that gets labeled schizophrenic is a special strategy that a person invents in order to live in an unlivable situation [author’s emphases]” (1967, pp. 114-115).
Bertram Karon, one of the world’s most renowned clinicians specializing in psychotherapy for those diagnosed with psychotic disorders, stated his belief that any one of us would also likely experience psychosis if we were to have to live through the same set of circumstances as those of his psychotic clients (Karon & VandenBos, 1996). We see other evidence of this again and again in the plethora of biographical and autobiographical accounts that have been written and filmed (for example, Bassman, 2007; Beers, 1981; Dorman, 2003; Greenberg, 1964; Modrow, 2003).
The focus of my own research (Williams, 2011, 2012) was to explore the change that takes place with regard to one’s experience and understanding of the world and one’s self (one’s personal paradigm) throughout the entire psychotic process, from onset to full recovery. The findings that emerged with regard to the onset of psychosis were very much in alignment with the findings of the other research mentioned above—there is clear evidence that every participant in all three of my own studies had also experienced such an overwhelming dilemma prior to the onset of psychosis. After thorough analysis of the data in the final and most comprehensive of the three studies, I arrived at the conclusion that there were essentially two fundamental dilemmas that appeared to lie at the crux of both the onset and resolution of these participants’ psychotic process:
The need to achieve a sustainable balance between autonomy (personal choice/personal freedom/authenticity) and connection (love/belonging/acceptance)
The need to maintain a relatively secure and stable sense of self when the very fabric of one’s being and indeed of the entire universe is profoundly groundless, impermanent, and interconnected.
What is particularly interesting about these dilemmas is that they may be the very same dilemmas that lie at the core of all human experience, regardless of one’s degree of sanity or lack thereof. It’s likely that most of us can easily relate to the first dilemma—we only need to think of the various challenges we’ve had in our relationships with family members, partners, and other loved ones. We can also easily witness this dilemma occurring within toddlers as they struggle to find a balance between the drive to explore the world and assert their autonomy while still wanting to be unconditionally loved and accepted by their caretakers. And of course this dilemma never fully goes away for most of us.
The second dilemma mentioned above is probably a little more difficult for some of us to relate to, especially for us Westerners (many practitioners of some of the Eastern traditions such as Buddhism, Taoism, and Advaita Vedanta have thoroughly explored this dilemma). This dilemma generally lies a little more deeply beneath our conscious awareness than the first dilemma, though it often becomes conscious in unusual circumstances, such as during psychological/emotional crisis, intensive contemplative practice (such as mindfulness meditation), and hallucinogenic drug use.
So, if these existential dilemmas are universal, then why do some individuals become more overwhelmed by them than others, and go on to develop psychosis?
The research suggests that there are two main factors that may make someone vulnerable to experiencing one or both of these dilemmas to a very high degree:
With regard to being overwhelmed by the first existential dilemma (that of finding a tolerable balance between autonomy and relationship), developmental and/or acute trauma appears to play a particularly strong role. It has long been established in the field of developmental psychology that healthy childhood development requires that we find a healthy balance between our sense of autonomy and our trust that we are loved and accepted by others.
Attachment research has been exploring and validating this idea for decades. Childhood abuse (physical, sexual, and/or emotional), trauma, neglect, and a poor fit between the temperament of a child and her/his caretaker(s) all clearly interfere with establishing a healthy balance in this regard, and all of these are well established in predisposing someone to developing serious emotional and psychological problems, and in more extreme cases, psychosis (Karen, 1994; Mahler, Pine, & Bergman, 1973; Rathus, 2006; Schore, 2002; Slade, 1999; Wallin, 2007; Williams, 2011, 2012).
Recall that the second existential dilemma refers to our need to maintain the sense that we are a relatively secure and stable self living in a relatively secure and stable world, when the reality of our situation is very different than this. To better understand how someone can be overwhelmed by this dilemma, it will help to first touch on the concept of cognitive constructs. The term cognitive constructs refers to the belief systems and interpretations that each of us has constructed throughout our lives which allow us to make sense of the world.
They can act somewhat like a double edged sword for us. On one hand, they provide us with the means to distinguish one object or being from another, and they give us the general sense that we “kinda know what’s going on” so that we can meet our needs and navigate our way through life. They also give us a sense that there is some solid ground beneath our experience—in other words, that we are a secure and stable self living in a relatively secure and stable world. But on the other hand, our cognitive constructs can close our minds to other perspectives, and they create the illusion that the world and our self are much more stable and secure than they actually are.
For most of us, our cognitive constructs are fairly solid, changing only slowly over time. However, in certain cases, such as during acute crisis or trauma, or with the use of certain psychoactive drugs, one’s cognitive constructs can become highly unstable. On one hand, this can lead to the potential benefit of having a more open mind (less rigid belief systems) and the richness of experiencing a greater sense of interconnectedness with all (more about this in my book, Rethinking Madness); but on the other hand, the loosening of our cognitive constructs can also lead to the potential terror of experiencing just how precarious and ungrounded our existence and self really are, which can lead to profound shifts within our personal paradigm as we desperately attempt to find some “solid ground” to cling onto once again. Such radical personal paradigm shifting is closely associated with anomalous experiences—so called delusions and hallucinations—experiences that are generally equated with psychosis.
Why some people are more prone to the loosening of one’s cognitive constructs is still somewhat mysterious—it appears that certain drugs and psychological or physiological distress may play a significant role, and some individuals may even have some genetic or developmental predisposition for such experiences. However, even though some people may be more prone to the destabilization of their cognitive constructs, it seems likely that virtually anyone has the potential to experience this if exposed to an overwhelming dilemma, situation, or trauma. It’s all too easy to find cases of extreme neglect, abuse, torture, or other trauma that have profoundly shaken up one’s experience of one’s self and the world and led to psychosis or at least psychotic-type experiences (those within the bottom three categories of Figure 3 above).
The research suggests, then, that both of these factors play an important role in the development of psychosis—an overwhelming existential dilemma and unstable cognitive constructs. The research also suggests that these two factors are very closely related, in that the experience of such an overwhelming dilemma makes one more susceptible to experiencing unstable cognitive constructs, and vice versa. It’s also important to emphasize that it is the individual’s own subjective experience of their situation that is most relevant. Sometimes, it’s easily evident to an observer that an individual is experiencing such an overwhelming dilemma (again, think of overt trauma, abuse, torture, etc.); but at other times, the individual’s crisis is not so apparent to an onlooker, though it is often all too apparent to the individual her/himself.
So, we finally arrive at the final and perhaps most important question in this discussion: “Why would an individual’s psyche intentionally initiate psychosis?”
In other words, how can something as chaotic and as potentially harmful as psychosis act as a strategy to aid someone in transcending an otherwise irresolvable dilemma? To understand this, it helps to use as a metaphor the process of metamorphosis that takes place within the development of a butterfly. In order for a poorly resourced larva to transform into the much more highly resourced butterfly, it must first disintegrate at a very profound level, its entire physical structure becoming little more than amorphous fluid, before it can reintegrate into the fully developed and much more resourced form of a butterfly.
In a similar way, when someone enters a state of psychosis, we can say that prior to the onset of psychosis, for whatever reason, they have arrived at a way of being in the world and experiencing of the world that is no longer sustainable (i.e., is poorly resourced), and it seems that their predicament cannot be resolved using more ordinary strategies. As a desperate last-resort strategy, then, one’s own psyche may initiate a psychotic process. As the individual enters into a psychotic process, we can say that their very self, right down to the most fundamental levels of their being, undergoes a process of profound disintegration; and as we have seen in the recovery research, with the proper conditions and support, there is every possibility of their continuing on to profound reintegration and eventual reemergence as a renewed self in a significantly changed and more resourced state than that which existed prior to the psychosis.
This is why the intentional destabilization of one’s cognitive constructs may be so beneficial, although of course very risky. It is this very loosening of one’s personal paradigm—of one’s experience and understanding of one’s self and of the world—that allows an individual to undergo such a profound transformation at such a deep level of their being. When such a process resolves successfully, the potential amount of growth and/or healing that this allows is enormous; but of course, when such a process does not resolve successfully, an individual’s personal paradigm may remain unstable and chaotic indefinitely (think florid psychosis).
This idea is well supported in the recovery research in the findings that many people who make full recoveries from psychosis often experience a degree of wellbeing and ability to meet their needs that far exceeds that which existed prior to their psychosis (Arieti, 1978; House, 2001; Karon & VandenBos, 1996; Laing, 1967; May, 1977; Mindell, 2008; Mosher, 1999; Mosher & Hendrix, 2004; Nixon et al., 2009, 2010; Perry, 1999; Williams, 2011, 2012). It’s important to keep in mind, of course, that such resolution is not always successful, and that an individual may remain in a psychotic condition indefinitely. But we must also not lose sight of the very hopeful findings from the recovery research that suggest that such a successful resolution from a psychotic process is surprisingly common, and may even be the most common outcome given the proper conditions and support (Hopper et al., 2007; Perry, 1999; Mosher, 1999; Mosher & Hendrix, 2004; Seikkula et al., 2006).
Finally, one particularly compelling implication of these findings is that if it turns out to be true that those who have experienced psychosis have struggled profoundly with the universal existential dilemmas that most of us have only barely consciously grasped, then these individuals may have the potential to contribute greatly to the very important human quest to understand what it is that really drives us.
Dr. Paris Williams, author of Rethinking Madness, works as a psychologist in the San Francisco Bay Area. He offers the rare perspective of someone who has experienced psychosis from both sides—as a researcher and psychologist, and as someone who has himself fully recovered after struggling with psychotic experiences. He can be reached at: www.RethinkingMadness.com/contact.
You can find a much more thorough discussion of these and related topics in Dr. Williams’ recently published book, “Rethinking Madness” (Sky’s Edge Publishing), which is available through Amazon.com and most other major retail outlets. More information is available at www.RethinkingMadness.com
American Psychiatric Association [APA]. (2010). Schizophrenia. Retrieved from The American Psychiatric Association Healthy Minds, Healthy Lives website: http://www.healthyminds.org/Main-Topic/Schizophrenia.aspx
Arieti, S. (1978). On schizophrenia, phobias, depression, psychotherapy, and the farther shores of psychiatry. New York, NY: Brunner/Mazel.
Bassman, R. (2007). A fight to be: A psychologist’s experience from both sides of the locked door. New York, NY: Tantamount Press.
Beck, J., and van der Kolk, B. (1987). Reports of childhood incest and current behavior of chronically hospitalized psychotic women. American Journal of Psychiatry, 29, 789-794.
Beers, C. W. (1981). A mind that found itself. Pittsburgh, PA: University of Pittsburgh Press.
British Psychological Society [BPS]. (2000). Recent advances in understanding mental illness and psychotic experiences. A report by The British Psychological Society Division of Clinical Psychology. Leicester, UK: Author.
Chadwick, P., Birchwood, M. J. & Trower, P. (1999). Cognitive therapy for delusions, voices and paranoia (Wiley series in clinical psychology). New York: John Wiley and Sons.
Dorman, D. (2003). Dante’s cure. New York, NY: Other Press.
Greenberg, J. (1964). I never promised you a rose garden. Chicago: Signet.
Hagen, B. F., Nixon, G., & Peters, T. (2010). The greater of two evils? How people with transformative psychotic experiences view psychotropic medications. Ethical Human Psychology and Psychiatry: An International Journal of Critical Inquiry, 12(1), 44-59.
Harrow, M., & Jobe, T. (2007). Factors involved in outcome and recovery in schizophrenia patients not on antipsychotic medications: A 15-year multifollow-up study. Journal of Nervous and Mental Disease, 195(5), 406-414. Retrieved from https://www.madinamerica.com/madinamerica.com/Schizophrenia_files/OutcomeFactors.pdf
Harrow, M., Jobe, T. H., & Faull, R. N. (2012). Do all schizophrenia patients need antipsychotic treatment continuously throughout their lifetime? A 20-year longitudinal study. Psychological Medicine, First View Articles, 1-11. doi: 10.1017/S0033291712000220
Honig, A., Romme, M., Ensink, B., Escher, S., Pennings, M., & de Vries, M. (1998). Auditory hallucinations: A comparison between patients and nonpatients. The Journal of Nervous and Mental Disease, 186, 646-651.
Hopper, K., Harrison, G., Janca, A., & Sartorius, N. (2007). Recovery from schizophrenia: An international perspective: A report from the WHO Collaborative Project, The International Study of schizophrenia. New York, NY: Oxford University Press
House, R. (2001). Psychopathology, psychosis and the kundalini: Postmodern perspectives on unusual subjective experience. In I. Clarke (Ed.), Psychosis and spirituality: Exploring the new frontier (pp. 75-89). London: Whurr Publishers.
Hyman, S., & Nestler, E. (1996). Initiation and adaptation: A paradigm for understanding psychotropic drug action. The American Journal of Psychiatry, 153(2), 151-162. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/8561194
Joseph, J. (2004). Schizophrenia and heredity: Why the emperor has no genes. In J. Read, L. R. Mosher, & R. P. Bentall (Eds.), Models of madness: Psychological, social and biological approaches to schizophrenia (pp. 67-83). New York, NY: Routledge.
Karen, R. K. (1994). Becoming attached: First relationships and how they shape our capacity to love. Oxford, UK: Oxford University Press.
Karon, B. P. (2003). The tragedy of schizophrenia without psychotherapy. Journal of the American Academy of Psychoanalysis, 31(1), 89-119. doi:10.1521/jaap.184.108.40.20631
Karon, B. P., & VandenBos, G. (1996). Psychotherapy of schizophrenia: The treatment of choice. Lanham, MD: Rowman & Littlefield Publishing, Inc.
Laing, R.D. (1967). The politics of experience. New York: Pantheon Books.
Lewine, R. (1998). Epilogue. In M. F. Lenzenweger & R. H. Dworkin (Eds.), Origin and development of schizophrenia (pp. 493-503). Washington, DC: American Psychological Association.
Livingston, R. (1987). Sexually and physically abused children. The Journal of the American Academy of Child and Adolescent Psychiatry, 26: 413-415.
Mahler, M. S., Pine, F., & Bergman, A. (1973). The psychological birth of the human infant, New York: Basic Books.
May, R. (1977). The meaning of anxiety. New York: W. W. Norton & Company.
Mindell. A. (2008). City shadows: Psychological interventions in psychiatry. New York, NY: Routledge.
Modrow, J. (2003). How to become a schizophrenic: The case against biological psychiatry. Lincoln, NE: Writers Club Press.
Mosher, L. R. (1999). Soteria and other alternatives to acute psychiatric hospitalization: A personal and professional review. The Journal of Nervous and Mental Disease, 187, 142-149.
Mosher. L. R., & Hendrix, V. (with Fort, D. C.) (2004). Soteria: Through madness to deliverance. USA: Authors.
National Institute of Mental Health [NIMH]. (2010a). Schizophrenia. Retrieved from http://www.nimh.nih.gov/health/publications/schizophrenia/complete-publication.shtml
National Institute of Mental Health [NIMH]. (2010b). How is schizophrenia treated. Retrieved from http://www.nimh.nih.gov/health/publications/schizophrenia/how-is-schizophrenia-treated.shtml
Nixon, G., Hagen, B. F., & Peters, T. (2009). Psychosis and transformation: A phenomenological inquiry. International Journal of Mental Health and Addiction. doi: 10.1007/s11469-009-9231-3
Nixon, G., Hagen, B. F., & Peters, T. (2010). Recovery from psychosis: A phenomenological inquiry. International Journal of Mental Health and Addiction. doi: 10.1007/s11469-010-9271-8
Perry, J. W. (1999). Trials of the visionary mind. State University of New York Press.
Rathus, S. A. (2006). Childhood and adolescence: Voyages in development. Belmont, Canada: Thompson Wadsworth.
Read, J. (2004). Biological psychiatry’s lost cause. In J. Read, L. R. Mosher, & R. P. Bentall, (Eds.), Models of madness: Psychological, social and biological approaches to schizophrenia (pp. 57-65). New York: Routledge.
Robins, L. (1974). Deviant children grown up: A sociological and psychiatric study of sociopathic personality. Malabar, FL: R. E. Krieger Pub. Co.
Romme, M., Escher, S., Dillon, J., Corstens, D., & Morris, M. (2009). Living with voices: 50 stories of recovery. Herfordshire, UK: PCCS Books.
Satcher, D. (1999). Etiology of schizophrenia. Retrieved, from http://www.surgeongeneral.gov/library/mentalhealth/chapter4/sec4_1.html
Schore, A. N. (2002). Advances in neuropsychoanalysis, attachment theory, and trauma research: Implications for self psychology. Psychoanalytic Inquiry, 22, 433-484.
Seikkula, J., Aaltonen, J., Alakare, B., Haarakangas, K., Keränen, J., & Lehtinen, K. (2006). Five-year experience of first-episode nonaffective psychosis in open-dialogue approach: Treatment principles, follow-up outcomes, and two case studies. Psychotherapy Research, 16(2), 214-228. doi: 10.1080/10503300500268490.
Siebert, A. (1999). Brain disease hypothesis for schizophrenia disconfirmed by all evidence. Retrieved from http://psychrights.org/states/Alaska/CaseOne/180Day/Exhibits/Wnotbraindisease.pdf
Slade, A. (1999). Attachment theory and research: Implications for the theory and practice of individual psychotherapy with adults. In J. Cassidy & P. R. Shaver (Eds.), Handbook of attachment: Theory, research, and clinical applications (pp. 575-594). New York: Guilford press.
Wallin, D. J. (2007). Attachment in psychotherapy. New York: The Guilford Press.
Whitaker, R. (2002). Mad in America. New York: Basic Books.
Williams, P. (2011). A multiple-case study exploring personal paradigm shifts throughout the psychotic process from onset to full recovery. (Doctoral dissertation, Saybrook Graduate School and Research Center, 2011). Retrieved from http://gradworks.umi.com/34/54/3454336.html
Williams, P. (2012). Rethinking madness: Towards a paradigm shift in our understanding and treatment of psychosis. San Francisco: Sky’s Edge Publishing.
Woodruff, P. W. R., & Lewis, S. (1996). Structural brain imaging in schizophrenia. In S. Lewis & N. Higgins (Eds.), Brain imaging in psychiatry. Oxford, UK: Blackwell.