“Full Recovery from Schizophrenia?”


By Paris Williams, PhD

 

This is the first of a series of blog postings related to my own series of research studies (my doctoral research at Saybrook University) of people who have made full and lasting medication-free recoveries after being diagnosed with schizophrenia and other psychotic disorders. This is very exciting research because it is one of the few areas within psychological research that remains almost completely wide open. One reason it is so wide open is that most Westerners don’t believe that genuine recovery from schizophrenia and other related psychotic disorders is possible, in spite of significant evidence to the contrary. Since there are some very hopeful findings that have emerged within this research, I want to begin this series of postings by summing up one particularly hopeful aspect of my own research, which is a group of five factors that emerged which are considered to have been the most important factors in my participants’ recovery process. But before looking closer at these factors, we should back up for a minute…

Upon reading the statement in the preceding paragraph, “…people who have made full and lasting medication-free recoveries from schizophrenia…,” it’s likely that many readers did a double-take. Yes, you read this correctly. Contrary to this widespread myth about schizophrenia, the research is quite robust in showing us that not only is full medication-free recovery from schizophrenia possible, it’s surprisingly common, and is actually themost common outcome in many situations—such as in many of the poorest countries of the world, such as India, Columbia, and Nigeria, and as the result of certain psychosocial interventions, such as the Open Dialogue Approach used in Lapland, Finland.

This is likely to come as a surprise to many because we simply don’t hear much about this in the mainstream media. In fact, we generally hear quite the opposite message repeated again and again in various forms — something to the effect of, “Schizophrenia is a degenerative brain disease from which full recovery is not possible.” Considering how robust the evidence is that full recovery is possible and actually quite common, coming from sources no less prestigious than the World Health Organization and the National Institute of Mental Health, it is really quite tragic that the myth of no recovery continues essentially unimpeded. But for now, rather than going further into the details of this recovery research (which is well documented in my book, Rethinking Madness), let’s return to the topic at hand — the factors that appear to be particularly important for those who have experienced such full and lasting recoveries:

Factor #1: Hope in the possibility of real recovery. All participants in all three of my research studies expressed that in order to even begin the journey towards real recovery, they first had to believe that such recovery is actually possible. And in order to do this, virtually all of them had to extract themselves from the intense hopelessness generated by the toxic (and untrue) belief that such recover is not possible — a belief that they all reported was forced upon them (quite heavily handed in most cases) within the mental health treatment that they had received.

This takes us to Factor #2: Arriving at an understanding of their psychosis alternative to the brain disease theory. Every participant went through a process of developing a more hopeful understanding of their psychotic experiences, generally coming to see their psychosis as a natural though very risky and haphazard process initiated by their psyche in an attempt to cope and/or heal from a way of being in the world that was simply no longer sustainable for them.

Factor #3: Finding meaning. All participants expressed how important it was for them to connect with meaningful goals/activities that made their life worth living—that provided them with some motivation to greet each new day with open arms and to channel their energy productively. And they all expressed having to overcome significant inhibition to this factor coming from the mainstream treatment they had received, which typically included strong motivation-inhibiting drugs (antipsychotics in particular) and the advice to generally lay low and avoid stress at all costs.

Factor #4: Connecting with their aliveness. All participants reported how important it was for them to connect more deeply with themselves—particularly with their feelings, needs, and sense of self agency. And again, they all reported finding significant hindrance to this factor coming from the mainstream treatment they had received—both from the inner conflicts arising from the belief of having a diseased brain as well as from the serious aliveness-dampening psychiatric drugs they were on.

Factor #5: Dealing with their relationships. All participants expressed the importance of healing and/or distancing themselves from unhealthy relationships and cultivating healthy ones. They all felt that unhealthy relationships played a significant role in their vulnerability to developing psychosis in the first place, and so this kind of work was extremely important. A number of them expressed gratitude to a therapist or friend who facilitated this work.

So, as we look at the sum total of these recovery factors, what we find is the rather disturbing idea that the mainstream paradigm of care for psychosis/schizophrenia may often cause more of a hindrance than a benefit in one’s recovery. In particular, there are two generally unquestioned aspects of the mainstream paradigm of care that should probably be seriously reconsidered:

(1) In spite of the widespread belief that one must remain on antipsychotics or similarly powerful psychiatric drugs for the duration of one’s life, the emerging recovery research reveals a very different picture. Not only have we discovered this in my own research, but the most recent longitudinal research conducted by the National Institute of Mental Health (no less) paints a very similar picture. This study essentially consisted of following a number of people diagnosed with schizophrenia in a non-interfering manner, simply allowing them to go about their lives in their own way, and allowing them to choose what kind of treatment they wanted. At the 15 year mark, it was found that of those who chose to stop taking their psychiatric drugs, 44% were considered “recovered,” compared to only 5% of those who have remained compliant with these prescriptions. This is a difference of nearly nine-fold in favor of those who stopped taking their prescribed psychiatric drugs. The World Health Organization studies have also shown in the so called “developing” countries in which psychiatric drug use is quite rare, well over half of those diagnosed with schizophrenia have gone on to make full recoveries, compared to only about a third of those in the U.S. and other so called “developed” countries, where psychiatric drug use is much more common.

So we find ourselves in quite a predicament. On one hand, it’s considered extremely dangerous to suggest that those diagnosed with schizophrenia should consider coming off these drugs, and even the mention of this possibility is considered one of the worst forms of taboo within the mental health field; but on the other hand, the research suggests that for many people, this is exactly what is called for. Of course, the research also shows that coming off these powerful drugs is very risky and should be done very slowly and under the careful guidance of a professional.

(2) Another major aspect of the mainstream treatment model that we find particularly problematic is the practice of trying to convince someone that they have a brain disease from which they will likely never recover. But the reality is that the brain-disease hypothesis remains unsubstantiated (see Rethinking Madness for a thorough discussion of this), and that full and lasting recovery is quite common. We also find that the hopelessness so often generated by this belief often leads to a self fulfilling prophecy — it appears to be very difficult to experience real recovery when you don’t believe it’s possible. Considering these points, then, it’s clear that we need to seriously reconsider the harm/benefit ratio of pushing these beliefs onto people and even the ethical implications of continuing to do so.

So we find ourselves at a crucial juncture in our treatment of people diagnosed with schizophrenia and other related psychotic disorders. We can take the path of least resistance, ignoring the results of the emerging recovery research, and carry on with treatment as usual, continuing to pay the ever increasing costs of this treatment model to society, the diagnosed individuals, and their families. Or we can take up the challenge of really embracing the emerging recovery research and its implications. This path will surely require a major overhaul of our mental health care system, but it offers the potential of significantly more hopeful outcomes for those so diagnosed as well as the greatly reduced burden on our increasingly struggling society as a greater percentage of people recover and regain the ability to take care of themselves. The choice is ours.

For a much more thorough discussion of these and closely related topics, as well as a detailed discussion of the finding of Dr. Williams’ own recovery research, you can find Dr. Williams’ book, Rethinking Madness (Sky’s Edge Publishing), on Amazon and other major retailers. More information is available at www.RethinkingMadness.com

References

Harrow M, & Jobe TH (2007). Factors involved in outcome and recovery in schizophrenia patients not on antipsychotic medications: a 15-year multifollow-up study. The Journal of nervous and mental disease, 195 (5), 406-14 PMID: 17502806

Harrow, M., Jobe, T., & Faull, R. (2012). Do all schizophrenia patients need antipsychotic treatment continuously throughout their lifetime? A 20-year longitudinal study Psychological Medicine, 1-11 DOI: 10.1017/S0033291712000220

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

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

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).

 

http://brainblogger.com/2012/06/23/is-schizophrenia-really-a-brain-disease/

Is Schizophrenia Really a Brain Disease?

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 hypothesis remain unsubstantiated, it has been directly countered by very well established 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 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 hypothesis. I’ll go through the largest 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 too 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(even though a significant degree of apathy towards one’s psychotic experiences often does kick in quickly, as would be expected with any kind of tranquilizer). 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.

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 (and virtually any psychoactive drug, for that matter) does lead to the development of a biochemical imbalance in one’s brain.

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 scrutiny 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, water retention, pregnancy, advancing age, variations in educational achievement, social class, ethnicity, and head size. 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. 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 affected by the long-term use of antipsychotic drugs.

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]”; 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.

Hypothesis #3: Schizophrenia is a Genetic Disorder

This hypothesis is in close alignment with the two brain disease hypotheses (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 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 maybe 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; another study found that 46% of women hospitalized for psychosis had been victims of incest; 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; 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. 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.

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”, 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”. Similarly, the American Psychiatric Association also confidently proclaims that “schizophrenia is a chronic brain disorder”, but then they acknowledge on the very same page that “scientists do not yet know which factors produce the illness”, and that “the origin of schizophrenia has not been identified”. 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”. It would appear, then, that it is simply not appropriate to claim with such confidence that schizophrenia is the result of a brain disorder.

If schizophrenia really is a brain disease, then how do we account for the relatively high rates of full recovery from it?

The recovery research is extremely robust: 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 and the World Health Organization. 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. 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, or multiple sclerosis: There is no well documented evidence of even a single individual making a full recovery from any of these well-established diseases of the brain.

The mainstream paradigm of care may actually be creating a self-fulfilling prophecy of brain disease

A tragic result of the entrenched belief that schizophrenia is caused by a disease of the brain is that, whether or not schizophrenia is ever determined to be a disease of the brain, our mainstream paradigm of care is actually ensuring that enormous numbers of people actually dodevelop such a disease (see the figure; I will also discuss this in more detail in a future blog).

So what does cause schizophrenia?

So, if schizophrenia is not caused by a disease of the brain, then the obvious question that arises is, “Well, then what does cause it?” This is an extremely important yet somewhat complex question, which I address in great detail in my book, Rethinking Madness, and which I will try to capture in a nutshell (or perhaps several nutshells) in future blog postings within this series.

For a much more thorough discussion of these and closely related topics, as well as a detailed discussion of the finding of Dr. Williams’ own recovery research, you can find Dr. Williams’ book, Rethinking Madness (Sky’s Edge Publishing), on Amazon and other major retailers. More information is available at www.RethinkingMadness.com

References

American Psychiatric Association [APA]. (2010). Schizophrenia. Healthy Minds, Healthy Lives [website].

Beck JC, & van der Kolk B (1987). Reports of childhood incest and current behavior of chronically hospitalized psychotic women. The American journal of psychiatry, 144 (11), 1474-6 PMID: 3674230

Harrow M, & Jobe TH (2007). Factors involved in outcome and recovery in schizophrenia patients not on antipsychotic medications: a 15-year multifollow-up study. The Journal of nervous and mental disease, 195 (5), 406-14 PMID: 17502806

Harrow M, Jobe TH, & Faull RN (2012). Do all schizophrenia patients need antipsychotic treatment continuously throughout their lifetime? A 20-year longitudinal study.Psychological medicine, 1-11 PMID: 22340278

Honig A, Romme MA, Ensink BJ, Escher SD, Pennings MH, & deVries MW (1998). Auditory hallucinations: a comparison between patients and nonpatients. The Journal of nervous and mental disease, 186 (10), 646-51 PMID: 9788642

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.

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.

Karon BP (2003). The tragedy of schizophrenia without psychotherapy. The journal of the American Academy of Psychoanalysis and Dynamic Psychiatry, 31 (1), 89-118 PMID:12722890

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.

Mosher LR (1999). Soteria and other alternatives to acute psychiatric hospitalization: a personal and professional review. The Journal of nervous and mental disease, 187 (3), 142-9 PMID: 10086470

National Institute of Mental Health [NIMH]. (2010a). Schizophrenia.

National Institute of Mental Health [NIMH]. (2010b). How is schizophrenia treated.

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.

Satcher, D. (1999). Etiology of schizophrenia.

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.

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.

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About annecwoodlen

I am a tenth generation American, descended from a family that has been working a farm that was deeded to us by William Penn. The country has changed around us but we have held true. I stand in my grandmother’s kitchen, look down the valley to her brother’s farm and see my great-great-great-great-great-grandmother Hannah standing on the porch. She is holding the baby, surrounded by four other children, and saying goodbye to her husband and oldest son who are going off to fight in the Revolutionary War. The war is twenty miles away and her husband will die fighting. We are not the Daughters of the American Revolution; we were its mothers. My father, Milton C. Woodlen, got his doctorate from Temple University in the 1940’s when—in his words—“a doctorate still meant something.” He became an education professor at West Chester State Teachers College, where my mother, Elizabeth Hope Copeland, had graduated. My mother raised four girls and one boy, of which I am the middle child. My parents are deceased and my siblings are estranged. My fiancé, Robert H. Dobrow, was a fighter pilot in the Marine Corps. In 1974, his plane crashed, his parachute did not open, and we buried him in a cemetery on Long Island. I could say a great deal about him, or nothing; there is no middle ground. I have loved other men; Bob was my soul mate. The single greatest determinate of who I am and what my life has been is that I inherited my father’s gene for bipolar disorder, type II. Associated with all bipolar disorders is executive dysfunction, a learning disability that interferes with the ability to sort and organize. Despite an I.Q. of 139, I failed twelve subjects and got expelled from high school and prep school. I attended Syracuse University and Onondaga Community College and got an associate’s degree after twenty-five years. I am nothing if not tenacious. Gifted with intelligence, constrained by disability, and compromised by depression, my employment was limited to entry level jobs. Being female in the 1960’s meant that I did office work—billing at the university library, calling out telegrams at Western Union, and filing papers at a law firm. During one decade, I worked at about a hundred different places as a temporary secretary. I worked for hospitals, banks, manufacturers and others, including the county government. I quit the District Attorney’s Office to manage a gas station; it was more honest work. After Bob’s death, I started taking antidepressants. Following doctor’s orders, I took them every day for twenty-six years. During that time, I attempted%2
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