Tag Archives: schizophrenia

A Macabre Celebration:  80 Years of Convulsive ‘Therapy’

There’s an interesting article in the June 2014 issue of the Journal of ECT.  It’s written by Max Fink, MD, and is titled Celebrating 80 Years of Inducing Brain Seizures as Psychiatric Treatment.  Dr. Fink is a psychiatrist and neurologist, and professor emeritus of psychiatry and neurology at the State University of New York, Stony Brook.

The article is short (approximately 400 words), and is essentially a tribute to Ladislas Meduna for his discovery  “…that induced seizures alleviated severe psychiatric disorders…”, which Dr. Fink describes as  “…a remarkable medical advance…”

Here are some quotes from the article, interspersed with my comments:

“When the Hungarian neuropathologist Ladislas Meduna found increased gliosis in the brains of epileptic patients and decreases in those with schizophrenia, he saw the illnesses as antagonistic and thought that inducing epileptic seizures might relieve psychosis.”

Glial cells are non-neuron brain cells.  In other words, they are not nerve cells.  Rather, they provide structure and support for the nerve cells.  Gliosis refers to a condition of the glial cells that occurs in response to damage.  The condition usually entails an increase in the number and size of the glial cells, and in extreme cases produces a scar.  Gliosis is associated with epilepsy, but it is unclear which is the cause and which is the effect.  What is clear, however, is that gliosis always has the potential to produce serious adverse effects.

In this context, there is an almost childlike naïveté to Dr. Meduna’s line of reasoning.  Essentially he has two groups of people:  those with epilepsy and those who have been “diagnosed with schizophrenia.”  On post-mortem examination, he finds relatively more scar tissue in the brains of the former group, and relatively less in the brains of the latter group.  He also had noticed that the incidence of epilepsy was low in people “diagnosed with schizophrenia.”  So, apparently, he reasons: the induction of grand mal seizures in the “schizophrenics” will have a therapeutic effect.  (Incidentally, given the low reliability of the label “schizophrenia,” the statement that the incidence of epilepsy was low in this group is fraught with problems.  But that’s another issue.)

The fact that epilepsy is a devastating illness and that grand mal seizures are clearly not benign occurrences doesn’t seem to have entered into Dr. Meduna’s reckoning.  He tried various chemicals to induce seizures in animals, and finally chose camphor.  Then, according to Wikipedia:

“For a population with severe schizophrenia, he moved from Budapest to the psychiatric hospital at Lipotmező, outside Budapest. He began his dose-finding experiments on January 2, 1934.” [Emphasis added]

Dr. Meduna later switched to pentylenetrazol (Metrazol), a stimulant drug which produces convulsions at high doses.

Incidentally, here’s a description of a Metrazol-induced seizure.  The quote is taken from Metrazol Therapy on the site fairfieldstatehospital.com.

“Metrazol produced an explosive seizure about a minute after the injection. Often these convulsions would result in fractured bones and torn muscles. For the therapy to be effective it would be given two or three times a week and a typical course of therapy would be thirty to forty injections. As the patient regained consciousness they would be confused and cooperative with staff which was seen as a marked improvement. Other times in this twilight state the patient would act in a more regressive manner, frightened and scared by the treatment. After a patient received one treatment they were resistant to subsequent treatment, resisting and pleading for it not to be done again and would have to be forcibly treated.”

And it is the inventor of this “treatment” that Dr. Fink wishes to honor!

. . . . . . . . . . . . . . . .

“In 1938, seizures using household electric currents replaced Metrazol, not for greater efficacy, but wholly for ease of use.  By the 1950s, grand mal seizures were being induced in thousands of patients in the main psychiatric treatment centers worldwide.”

ECT was first used by Ugo Cerletti, MD, in 1938, in Rome.  Here’s a description, written by Dr. Cerletti himself, of the first use of this “therapy”:

“A schizophrenic of about forty, whose condition was organically sound, was chosen for the first test. He expressed himself exclusively in an incomprehensible gibberish made up of odd neologisms, and since his arrival from Milan by train without a ticket, not a thing had been ascertainable about his identity.

Preparations for the experiment were carried out in an atmosphere of fearful silence bordering on disapproval in the presence of various assistants belonging to the clinic and some outside doctors.

As was our custom with dogs, Bini and I fixed the two electrodes, well wetted in salt solution, by an elastic band to the patient’s temples. As a precaution, for our first test, we used a reduced tension (seventy volts) with a duration of 0 2 second. Upon closing the circuit, there was a sudden jump of the patient on his bed with a very short tensing of all his muscles; then he immediately collapsed onto the bed without loss of consciousness. The patient presently started to sing at the top of his voice, then fell silent. It was evident from our long experience with dogs that the voltage had been held too low.

I, bearing in mind the observations with repeated applications of the day before upon pigs, made arrangements for a repetition of the test.

Someone got nervous and suggested whisperingly that the subject be allowed to rest; others advised a new application to be put off to the morrow. Our patient sat quietly in bed, looking about him. Then, of a sudden, hearing the low toned conversation around him, he exclaimed – no longer in his incomprehensible jargon, but in so many clear words and in a solemn tone – ‘Not a second. Deadly! ‘

The situation was such, weighted as it was with responsibility, that this warning, explicit and unequivocal, shook the persons present to the extent that some began to insist upon suspension of the proceedings, Anxiety lest something that amounted to superstition should interfere with my decision urged me on to action. I had the electrodes reapplied, and a 110-volt discharge was sent through for 0.5 second. The immediate, very brief cramping of all the muscles was again seen; after a slight pause, the most typical epileptic fit began to take place. True it is that all had their hearts in their mouths and were truly oppressed during the tonic phase with apnea, ashy paleness, and cadaverous facial cyanosis – an apnea which, if it be awe-inspiring in a spontaneous epileptic fit, now seemed painfully never-ending – until at the first deep, stertorous inhalation, and first clonic shudders, the blood ran more freely in the bystanders’ veins as well; and, lastly, to the immense relief of all concerned, was witnessed a characteristic, gradual awakening ‘by steps’. The patient sat up of his own accord, looked about him calmly with a vague smile, as though asking what was expected of him. I asked him: ‘What has been happening to you?’ He answered, with no more gibberish: ‘I don’t know; perhaps I have been asleep.'”

Note how Dr. Cerletti dismisses as “superstition” the notion that the victim’s prohibition (‘Not a second.  Deadly’) should be taken seriously.  And when Dr. Fink writes that electricity replaced Metrazol “…for ease of use,” he probably was not talking about the client’s ease.

The great tragedy of all this is that the “improvements” noted following electric shock convulsions are similar to, and essentially instances of, the transient state of euphoria and compliance that frequently follows severe head injury.

. . . . . . . . . . . . . . . .

“Widespread belief that electricity caused brain damage and persistent memory loss stigmatized the treatment.”

Note the word “belief” and the suggestion that these “beliefs” were unfounded.  In other writings, Dr. Fink has been more direct.  On October 1, 2006, for instance, he wrote an article for Psychiatric Times called The Camelford Hysteria: A Lesson for ECT?  In this piece, he states clearly:

“Complaints of persistent memory loss in otherwise well-functioning individuals after recovery from a psychiatric illness through ECT are best viewed as a conversion reaction or a somatoform disorder.”

In other words, if my readers will pardon the expression, the memory loss is all in their heads!  Psychiatry is a great disrespecter of people, but this statement of Dr. Fink’s must surely take the proverbial biscuit.

Back to the Celebrating 80 Years article.

“For more than half a century, our research interest focused on minimizing electricity’s hazards.  Electrode placement, electricity form and energy dosing were repeatedly tested, but no modification was without complaint.”

This strikes me as an interesting way to spend 50 years, if in fact the hazards were nothing more than the manifestations of victims’ neurotic imaginations.

. . . . . . . . . . . . . . . .

 “Meduna’s hypothesis that seizures, not the method of induction, were the basis for remission was repeatedly verified”

“An alternative to electricity using the inhalant anesthetic flurothyl is of renewed interest.”

And finally:

“Ladislas Meduna’s demonstration that induced seizures alleviated severe psychiatric disorders was a remarkable medical advance that developed despite universal fears of epilepsy and of electricity.  Although little heralded, the remissions of the illnesses of many hundreds of thousands of the severely ill justify the celebration of this remarkable discovery.”

In fact, however, electric shock “treatment” is no more effective than sham ECT, in which the client is prepared and anaesthetized, but not actually shocked (Bracken et al, 2012)

When one considers the pains to which real doctors go to protect their patients from seizures, I suggest that the deliberate induction of grand mal seizures, often involuntarily, constitutes neither “a remarkable discovery” nor a “remarkable medical advance,” but rather aggravated assault by a person in a position of trust.

In September 2005, Dr. Fink was interviewed by Arline Kaplan Long, and the interview was written up in Psychiatric Times.  Here’s a quote from the article:

“Asked what he wants psychiatrists and others to understand about ECT, Fink responded, ‘Over the 70-plus years that ECT has been around, we have learned to appreciate that something magical happens in the body when we produce an epileptic fit.'”

And here, dear readers, I have to confess that words fail me!

Childhood Social Functioning Predicts Adult Schizophrenia Spectrum Disorder. Or Does It?

In November 2013, the journal Schizophrenia Research published a paper by Tsuji, T. et al. titled Premorbid teacher-rated social functioning predicts adult schizophrenia-spectrum disorder: A high-risk prospective investigation.  Here’s the abstract:

“Social functioning deficits are a core component of schizophrenia spectrum disorders, and may emerge years prior to the onset of diagnosable illness. The current study prospectively examines the relation between teacher-rated childhood social dysfunction and later mental illness among participants who were at genetic high-risk for schizophrenia and controls (n=244). The teacher-rated social functioning scale significantly predicted psychiatric outcomes (schizophrenia-spectrum vs. other psychiatric disorder vs. no mental illness). Poor premorbid social functioning appears to constitute a marker of illness vulnerability and may also function as a chronic stressor potentially exacerbating risk for illness.”

The study was done in Denmark by a Danish-American team, as part of a large scale longitudinal developmental study.  Studies of this sort are often done in Denmark, incidentally, because the Danes have a central mental health register and other data bases that facilitate the gathering of follow-up information.

The social functioning measure consisted of five items, each of which was rated on a five point scale.  The total score was obtained by adding the five individual item scores.  Lowest possible score was 5; highest possible score was 25.  The items were:

1. The child does not seem to take part when the rest of the class is having fun.
2. The child has no friends.
3. The child is often teased.
4. The child does not actively seek friends.
5. The child seems to avoid contact with other children.

Here are some more quotes, interspersed with my comments:

“Results suggest that, even though many psychiatric difficulties are associated with deteriorations in social functioning, teacher-rated social deficits among school-age children appear to represent a marker of vulnerability specific to disorders within the ‘family’ of schizophrenia spectrum illnesses. These findings highlight the value of teachers in identifying key markers of risk such as social deficits.”

In the abstract quoted earlier, the authors acknowledge that “social functioning deficits are a core component of schizophrenia spectrum disorders.” [Emphasis added]  With this in mind, it seems to me that the best and most parsimonious way to conceptualize the research finding is that children who have poor social skills will, in many cases, grow up to be adults with poor social skills.  In particular, there seems to me no justification (other than psychiatric dogmatism) to conceptualize the matter in medical terms, and to impose a medical framework – “a marker of vulnerability” – on the data.

“Thus, social functioning has emerged as an important area for researchers interested in the core features of emerging psychotic illness…”

Here again, note the assumption of an “emerging…illness.”

“…results from this 48-year longitudinal record suggest that children on a trajectory toward schizophrenia-spectrum disorders demonstrate interpersonal deficits early in life, and that teachers provide valuable information regarding children’s social functioning.”

Again, note the medical language:  children with poor social skills are “on a trajectory toward schizophrenia spectrum disorders.”  The term “on a trajectory” also entails an element of inevitability, implying that children with poor social skills become psychotic in the same way that people who inherit the Tay-Sachs gene get the disease.  Note also the identification of teachers as sources of “valuable information.”

A follow-up period of 48 years (1959-2007) is impressive in a longitudinal study, and it is likely that the findings will be afforded a high measure of credibility and status within the psychiatric community.  A Google search on May 14 for the title got 7,770 hits.  So the study is attracting attention.

In recent years, organized psychiatry has been actively promoting the notion of early intervention in schools and other settings for people who are considered “at risk” for acquiring a diagnosis of schizophrenia (e.g. here and here).  The DSM-5 workgroup promoted the “diagnosis” of attenuated psychosis syndrome, as a means of identifying teens considered to be “at risk,”  and this “diagnosis” is included in the manual as a specific example in the category:  “Other Specified Schizophrenia Spectrum and Other Psychotic Disorder 298.8” (p 122).

In this general context, a simple (5-item) teacher-completed social skills rating scale is likely to have considerable appeal.  For these reasons, it seems important to subject the study to some scrutiny.


Perhaps the study’s most significant shortcoming is the one already mentioned:  that poor social skills are in fact the primary defining feature of DSM-5’s “schizophrenia spectrum and other psychotic disorders.”  The defining features of these psychiatric “diagnoses” are set out on pages 87 and 88 of the manual, and include the following, all of which fall, I suggest, under the heading of social skills deficits:

    • reduction in the expression of emotions in the face
    • showing little interest in…social activities
    • diminished speech output
    • lack of interest in social interactions
    • childlike silliness
    • lack of verbal…responses
    • staring
    • grimacing
    • mutism
    • echoing of speech
    • switching topics

Even delusions and hallucinations, the cornerstones of these “diagnoses,” are closely connected to social skills. A child who grows up with poor social skills is often victimized and bullied, and quickly learns that the “real” world is not usually a source of joy or reward.  The subsequent retreat into a private realm is not only understandable, but in many cases adaptive.

So when Tsuji et al. discovered, through their research, that children who are rated by their teachers as socially unskilled, have a better than average chance of attracting a “diagnosis” of a schizophrenia spectrum disorder in adulthood, all that they have found is that some individuals, who are socially unskilled as children, are socially unskilled in adulthood.  Poor social skills is an inherent component of the definition of “schizophrenia.”  The notion that this needs to be discovered as a “marker of vulnerability” is specious and misleading.


The study write-up is sparse in both description and data, so it’s not possible to subject the numbers to serious scrutiny.  But it is clear that many of the participants who were rated poor on social skills during childhood grew up to have “no mental illness” in later life.  The authors do tell us that the “…[s]ocial functioning scores ranged from 6 to 25 with an overall sample mean of 20.83 (SD = 3.78).”  They also provide means and standard deviations for the three outcome groups.

chart 1 May 14






It should be noted that the above table does not appear in the text, but was created by me from data presented as run-on text in three separate sections of the paper.  (Higher scores mean better social functioning)

What’s immediately clear from this table is that there is considerable overlap in the social skills scores from the three outcome groups.  We can get an estimate of the range of the three groups from the standard deviations.  Most of the participants’ scores will lie in the range from two SD’s below the mean to two SD’s above the mean.  So we can calculate tentative score ranges as follows:  (The range for all scores was 6-25, so 25 is always the upper limit.)

Chart 2 May 14







It is reasonably certain that many of the low scorers in the NMI group scored below the mean of the schizophrenia spectrum group, and yet these individuals had never been assigned a mental illness “diagnosis” of any kind.  It’s not possible to say, based on the published data, what the absolute numbers were, but given that the NMI group is four times larger (133 vs. 33) than the spectrum group, it is entirely feasible that there were as many, or even more, individuals in the NMI group scoring below the “spectrum” mean (17.55) as there were in the spectrum group.  Using the spectrum mean (17.55) as a prognostic cutoff would have created the prediction that these individuals were on the so-called trajectory to a schizophrenia spectrum disorder.  But in fact they acquired no mental health “diagnoses” at all.  So using this social skills scale, or indeed any similar scale, is likely to “identify,” and target for psychiatric treatment, large numbers of individuals who in fact were “on a trajectory” to “no mental illness.”

And there’s another problem.  Of the 33 individuals who received a diagnosis of a schizophrenia spectrum disorder in adulthood, only 18 of these had been assigned a diagnosis of schizophrenia.  The remaining “diagnoses” were:

Psychosis NOS or delusional disorder                                    8

Schizotypal, paranoid, and schizoid personality disorder      7

The authors state that their decision to group these categories together was “…guided by familial research suggesting genetic links between the disorders…”  However, it is entirely possible that the grouping was done to increase the size of the high “pathology” group in order to make the association seem more robust.  It is also possible that the data was pre-examined and it was noticed that a large proportion of the poor-social-skills group had been assigned these other diagnoses in adulthood.

I have no way of knowing if any data massaging of this sort happened.  But the decision to group the diagnoses in this way, coupled with the sparseness of data in the write up, raises questions.  At the very least, it increases the chances of a predictive “hit” by the simple expedient of widening the target.

Another troubling aspect of the “diagnosis” grouping is that the authors are not using the term “schizophrenia spectrum disorders” in the same sense as DSM-5.  In particular, the authors have included the conditions known as paranoid and schizoid personality disorders, neither of which is included in the DSM-5 grouping.  This, I suggest, is important for two reasons.  Firstly, most readers on coming across this term in the title and in the abstract, would have assumed that it referred to the DSM-5 category.  At the very least, the authors should have stated explicitly that this is not the case – that in fact, they were using the term differently.  Secondly, and more importantly, the behaviors entailed in the paranoid personality and schizoid personality labels are entirely a function of social skills.  It is likely that individuals who meet these general descriptors would score very low on a social skills scale at age 11-13, and this may have been a major factor in depressing the overall score of the spectrum group.

Many credible accusations of data massage have been leveled at psychiatric researchers in recent years, and in this regard it would have been helpful if Tsuji et al. had published some more numerical data. Even the means and standard deviations of the “paranoid” and “schizoid” personality groups would have been useful.


As mentioned earlier, the title of the article is Premorbid teacher-rated social functioning predicts adult schizophrenia-spectrum disorder: A high-risk prospective investigation.

This, I suggest, is misleading.  The social functioning risk ratio for no mental illness vs. spectrum disorders was only 1.31 (with a 95% confidence interval of 1.17 to 1.46).  This does not indicate high predictive potential.  To illustrate this, imagine 100 envelopes spread out on a large table; 50 red and 50 blue.  A person is informed (truthfully) that half of the blue envelopes contain a $100 bill and the other half contain a go-to-jail-now card.  With the red envelopes, the odds are better – 19 jail cards and 31 $100 bills.  The person is invited to choose one envelope and open it.  If it is a jail card, he will be incarcerated.  If it contains a $100 bill, he gets to keep it.  Obviously, other things being equal, he should choose a red envelope, but he still runs a 38% chance of going to jail, versus a 50% with the blue envelopes.  The risk ratio for blue to red is about 1.31.  So, yes, the color red does predict dollars over jail – but the potential for error (i.e., jail) is still high.  Similarly, if a person were to use the five item social skills scale described in this study to predict a “schizophrenia spectrum disorder” in adulthood (odds ratio also 1.31), his prediction would be false a great deal of the time.  The word “significantly” in the abstract refers only to statistical significance, and indicates that the result is unlikely to have occurred by chance.  It has no bearing on the magnitude of the effect.

A more accurate title for the paper would be:

“Teacher-rated social functioning at age 10-13 (as measured by a five-item scale) is correlated modestly with acquiring a diagnosis of schizophrenia, or psychosis not otherwise specified or delusional disorder or schizotypal personality disorder or paranoid personality disorder or schizoid personality disorder, in adulthood.”


The great tragedy in this area is that poor social skills is an eminently remediable condition.  Social skills can be taught as easily, and as readily, as counting, spelling, and playing simple games.  Children, for instance, who are excessively boastful, which in later life will attract the label “grandiosity,” can be coached successfully to downplay their self-promotion and to pay compliments to others.  Ordinary conversational skills such as making eye contact, admitting to mistakes, smiling, allowing others an opportunity to speak,  etc., can all be coached without difficulty.  Conscientious parents have been doing this since the dawn of civilization, and probably even earlier.

Unfortunately, however, in the present time this kind of teaching often doesn’t take place.  While children who can’t count or read attract lots of remedial attention, the lack of social skills is somehow seen as an inherent defect that doesn’t lend itself to coaching.  Social skills are often conceptualized, even by teachers, as an integral part of “the child’s personality,” or as indicators of “deeper” problems, rather than skills that can be acquired, practiced, and cultivated in the normal way.  Children with deficits in this area are often sent to the mental health center, where they acquire various “diagnoses,” and are given the false and disempowering message that they are sick.  The Tsuji et al. study will lend unwarranted credence and support to this practice, in that it will be used to promote the notion that these individuals are “on a trajectory” to a “schizophrenia spectrum disorder,” and that this “trajectory” can be altered only by timely psychiatric intervention.

It is also the case that some people, children and adults, don’t want to socialize.  They prefer their own company, and often excel in various non-social areas.  The present drive towards “early intervention” will pathologize these individuals, and will draw them into psychiatry’s disempowering and destructive net – for their own good, of course.


Although Thomas Tsuji (a sixth-year grad student in the UBMC Department of Psychology) is shown as first author, it is clear the Jason Schiffman, PhD, is the principal investigator.  Under the heading “contributors,” the article states:  “Dr. Schiffman formulated, conducted, and/or oversaw the study design, data analysis, data interpretation and manuscript preparation.”  Dr. Schiffman is also listed as the “corresponding author,” with an address at the University of Maryland, Baltimore County (UMBC).  You can see his UMBC bio here.  His listed research interests are:  “Early identification and treatment of youth at risk for psychosis.  Reduction of stigma against people with serious mental health concerns.”

Some of Dr. Schiffman’s recent research publications are also listed.  Here are two quotes from these studies:

“Brief self-report questionnaires that assess attenuated psychotic symptoms have the potential to screen many people who may benefit from clinical monitoring, further evaluation, or early intervention.” (here)

“The validation of attenuated symptoms screening tools is an important step toward enabling early, wide-reaching identification of individuals on a course toward psychotic illness.” (here)

Dr. Schiffman is also on the staff of the Center for Excellence on Early Intervention for Serious Mental Illness.  This agency was created last year by a $1.2 M grant from the State of Maryland as part of the state’s response to the problem of mass shootings in schools and other locations.  The center is headed by Robert Buchanan, MD, a professor of psychiatry at University of Maryland.  Dollars for Docs indicates that Dr. Buchanan received $34,520 from pharma in the period 2009-2012.  Information on the Center’s activities to date is sparse, but I did find two Baltimore Sun articles about the Center.  The first article, titled New Maryland mental health initiative focuses on identifying and treating psychosis by Jonathan Pitts, was published on October 21, 2013.  Here are two quotes:

“Research has shown those who eventually develop psychosis have often exhibited early warning signs, clues that give family members, teachers, health-care providers and others a chance to intervene early, if only they know what to look for.”

“The Clinical High-Risk program will be contacting schools, houses of worship, law enforcement and other communities that come into contact with youth to promote public awareness about such signs, Schiffman said, and clinicians will be available to provide testing and offer treatment options.”

 The second article, written by Jean Marbella, was published on March 21, 2014.  It’s titled UMBC study among efforts to increase awareness of mental illness.  Here are some quotes:

 “‘Many of the folks who need help get lost somehow,’ said Jason Schiffman, an associate professor of psychology at the University of Maryland, Baltimore County who is heading the study. ‘There are so many kids and young adults who slip through the cracks.'”

 “Schiffman has long been interested in early intervention and de-stigmatization programs for those suffering mental health problems, but more recently, his work is benefiting from a new focus on the role such illnesses may have played in some shootings.”

 And perhaps most telling of all:

“‘As a society, if we normalize the seeking of help,” he said, “people are more likely to seek that help.'”

There is it:  psychiatry for all.  A “diagnosis” for every problem and a pill for every “diagnosis.”


And so it goes.  Psychiatry, reeling under an ever-increasing barrage of criticism, has taken nothing on board with regards to its spurious concepts and its destructive treatments.  Instead, it has hired a PR firm to polish up its image, and is actively cultivating the media and the politicians, with a view to embedding its concepts and practices more deeply into the legal and social fabric of our society.  It is also exploiting shamelessly the public concern about the mass murders to promote its own expansionist agenda, indifferent to the stigmatizing effect that this will have on millions of innocent, socially isolated teenagers..

A great deal of their present effort is directed at two main themes:  integration of psychiatry with primary care (a mental health worker in every GP’s office), and early intervention.  Watch out for media infomercials on these topics in your local newspapers, and for bills on these topics in your statehouses.  And please speak out.  Early intervention is just a catch-phrase to sell more drugs to children and to destroy more lives.

. . . . . . . . . . . . . . . 


In critiquing a paper like Tsuji et al., it is difficult to avoid using psychiatry’s terminology.  My use of the terms “schizophrenia,” “schizoid personality disorder”, “schizophrenia spectrum disorders,” etc. should not be taken to imply any endorsement on my part of the validity of these concepts.  On the contrary, the central theme of this website is that these terms have no ontological or explanatory significance, and are nothing more than loosely defined labels which psychiatry uses and promotes to legitimize the prescription of psychiatric drugs.

 Another Critique of the Schizophrenia Diagnosis

In January 2014, the journal Research on Social Work Practice ran a special issue called A Critical Appraisal of the DSM-5: Social Work Perspectives.  There are fifteen articles on this general theme, and together they present a wide range of arguments against the DSM system.

Social workers represent the numerically biggest group of mental health practitioners in the US, and it is particularly gratifying to see a major social work journal addressing this topic so forthrightly.

In this post, I want to focus on one of the articles:  A Critique of the Diagnostic Construct Schizophrenia, by Stephen Wong, PhD, BCBA-D, of the Florida International University in Miami.

Here are some quotes:

“Characterizing the many emotional, behavioral, functional, and social concerns listed in the manual as physical ‘diseases’ is a theoretical and ideological assertion.  And even though this assertion is repeated endlessly in professional and commercial media, the claim rests on faulty definitions, logical fallacies, and weak empirical evidence (Boyle, 2002; Moncrieff, 2008; Read, Mosher, & Bentall, 2004; Valenstein, 1998)”

“Equipped with the knowledge of these and other therapeutic techniques, social workers can take a more active role in the design and implementation of effective psychosocial interventions, rather than being handmaidens of psychiatrists and relying on the finite benefits of their pharmacological treatments (Cohen, 1997; Harrow & Job, 2007; Hegarty, Baldessarini, Tohen, Watternaux & Oepen, 1994; Whitaker, 2010).”

“While current mental health services focus primarily on treating unconfirmed biological or neurological diseases (Gomory, Wong, Cohen, & Lacasse, 2011; Kingdon & Young, 2007; Whitaker, 2010), social workers and other mental health professionals should not confine themselves to this narrow, reductionist perspective and should be sensitive to other factors contributing to severe mental and behavioral disturbances.”

“There is abundant research on environmental and social adversity factors contributing to the development of schizophrenic symptoms and psychosis to guide our practice in social advocacy, prevention, and treatment of mental and behavioral disorders.”

“The biggest question is, given the many conceptual, scientific, and technical shortcomings of the diagnosis of schizophrenia, and of DSM diagnoses in general, why are social workers, psychologists, and other mental health professionals so dutiful in their use of the DSM and not more outspoken in their criticism of these psychiatric labels?”

“However, simply acquiescing to this medical ideology also has direct consequences for individual clinicians and their professions.  For social workers, it means putting aside our person-in-the-environment approach, our appreciation of how life experiences and living conditions shape peoples’ thoughts and actions, and our professional independence.”

“Open criticism and resistance to the DSM would be a fitting starting point for organizing and opposing medical dominance and the biomedical hegemony over mental health services, and thereby better assisting members of our society with mental, emotional, and behavioral disturbances.”

I found Dr. Wong’s paper particularly encouraging not only for its intrinsic merit, but also for its rallying call to social workers to distance themselves from the DSM and from the concept of psychiatric illness generally.

I have often expressed the belief that a grassroots rebellion within the social work profession could be the tipping point in the marginalization of psychiatry, and in the development of an effective and truly person-centered framework for helping people in distress.


A Blood Test for Schizophrenia with 83% Accuracy?


An NBC online News article dated October 15, 2010, carried the noteworthy title New blood test may help detect schizophreniaThanks to Francesca for the link.

The article was written by Natasha Allen, a freelance medical journalist.  The gist of the article is that there is a new blood test called VeriPsych which “researchers say” is 83% accurate in discriminating people who are “schizophrenic” from people who are not.

One of the researchers – Michael Spain, MD, Chief Medical Officer of Rules-Based Medicine, is quoted as saying:

“There is a certain amount of denial when a child is diagnosed with schizophrenia. You wish that your child did not have that…It is a good test to convince parents or even the patient to stay on medication, as opposed to just subjective opinion.” [Emphasis added]

The article also points out that Rules-Based Medicine is the company that makes the test and funded the study.

The study itself is published in Biomarker Insights, a peer-reviewed journal that began publishing in 2006 and is owned by Libertas Academia.  The study appeared in the May 2010 issue and is called Validation of a Blood-Based Laboratory Test to Aid in the Confirmation of a Diagnosis of Schizophrenia. There are 24 authors.  The lead author is Emanuel Schwarz of the Institute of Biotechnology, University of Cambridge, UK.  The Institute of Biotechnology had reportedly served as consultants to Rules-Based Medicine.  Five other authors, including Sabine Bahn, MD, PhD, MRCPsych, have links to the Institute.

An additional four authors, including Dr. Spain, report links to Rules-Based Medicine Inc.

Another author reports links to Psynova Neurotech Ltd., Cambridge, UK (a subsidiary of Rules-Based Medicine).  And another reports links to the Stanley Medical Research Institute, Chevy Chase, Maryland.

Here’s the study’s abstract:

“We describe the validation of a serum-based test developed by Rules-Based Medicine which can be used to help confirm the diagnosis of schizophrenia. In preliminary studies using multiplex immunoassay profiling technology, we identified a disease signature comprised of 51 analytes which could distinguish schizophrenia (n = 250) from control (n = 230) subjects. In the next stage, these analytes were developed as a refined 51-plex immunoassay panel for validation using a large independent cohort of schizophrenia (n = 577) and control (n = 229) subjects. The resulting test yielded an overall sensitivity of 83% and specificity of 83% with a receiver operating characteristic area under the curve (ROC-AUC) of 89%. These 51 immunoassays and the associated decision rule delivered a sensitive and specific prediction for the presence of schizophrenia in patients compared to matched healthy controls.”

Which means that if you perform these 51 tests on a person’s blood and collate the results using VeriPsych’s algorithm, the result will predict schizophrenia with 83% accuracy.

In the conclusions section of the article it states:

“In this multicenter study, we discovered and validated a biomarker panel for schizophrenia based on biological and technical reproducibility of the molecular signature.”

“High classification performance demonstrated that the decision rule could identify schizophrenia patients with high accuracy irrespective of the disease duration or treatment state.”

“In summary, the present findings demonstrate the applicability of a rapid and non-invasive test to confirm the presence of schizophrenia.”

And their work is not finished!

“We anticipate that the 51-plex assay panel will result in the future development of a differential diagnostic test that can distinguish among various neuropsychiatric disorders such as schizophrenia, bipolar disorder and major depressive disorder.”

Under “Acknowledgement,” the authors tell us that the study was “instigated and supported” by:

  • Rules-Based Medicine
  • Psynova Neurotech Ltd
  • Stanley Medical Research Institute 

The authors express their thanks to various colleagues who assisted in the research.  And they singled out for special thanks “…Dr. Fuller Torrey for his support and suggestions.”


After the research article was published, the information about VeriPsych was picked up by the following media sources:

October 6 2010, a site called MPR put up a sort of ad that reads “VeriPsych schizophrenia diagnostic aid available,” and gives a number to call RBM for more info.

A site called Fast Company put up an article called Veripsych Says It Can Spot Depression, Schizophrenia In Blood on their site, no date given.

Singularity Hub put up an article Blood Tests to Diagnose Schizophrenia, Other Brain Disorders on the Horizon, by Jeremy Ford on Jan 18, 2011.

On October 13, 2010, livescience put up Natasha Allen’s article under the title It’s in the Blood: New Hope for Detecting Schizophrenia.  Here Ms. Allen is listed as a MyHealthNewsDaily Contributor.

Mental Healthy (UK) site ran an article Blood Test to diagnose schizophrenia and depression by Catherine Walker (probably in 2011), after Dr. Sabine made a presentation at the 2011 APA annual conference.

Psychiatric Times ran the headline Blood Tests for Diagnosis of Schizophrenia and Depression? on August 10, 2011

But three months later, on November 8, 2011, they also put up an article called Blood Tests for Diagnosis of Schizophrenia and Depression: Not Ready for Prime Time.

On October 28, 2012, Oxbridge Biotech Roundtable put out an article An afternoon with Prof. Sabine Bahn: Bridging prognosis, diagnosis and treatment.

Bipolar burble (a blog) did a post on this on April 18, 2011.  But the author of the blog put this at the end:

“This is a money-grab taking advantage of desperate mentally ill people.

I actually find this ‘diagnostic aid’ blood test for schizophrenia to be bordering on unethical. VeriPsych can cover their ass with math and statistics and probabilities and legal-eze and I’m sure that makes it ‘OK,’ but if you ask me, they are a hair’s breath away from lying. It feels irresponsible to me to hand out these kinds of results about a very serious illness based on one study. One. And there is so much math needed to make this model work that I would fall down dead if there wasn’t a mistake in there somewhere. Nobody gets it right the first time.”

 So we have a blood test for schizophrenia!  The Holy Grail – at last.  Schizophrenia, the darling “diagnosis” of psychiatry, can now take its rightful place in the halls of medicine, soon to be followed by bipolar disorder and major depressive disorder.  And disgruntled, misanthropic naysayers, such as myself, can slink cringingly into our narrow beds of shame and ignominy.


On January 2, 2013, the following notice appeared on VeriPsych’s website.  (VeriPsych is the name of the blood test, but it is also the name of the company that marketed the test and is affiliated with Rules-Based Medicine, which apparently is now called Myriad Rules-Based Medicine.)

“Thank you for visiting the VeriPsych website and for your interest in VeriPsych, the first blood-based diagnostic aid for schizophrenia.

 We have temporarily suspended offering the VeriPsych test in an effort to improve its utility. In 2010, we conducted a beta launch confirming that the test worked as intended; however, in close collaboration with our medical and scientific partners, we collectively determined that the product needed further refinement to better fit the needs of patients and healthcare providers. Accordingly, we have shifted our focus onto the development of new transformative molecular diagnostic tools that address bi-polar disorder and major depression, in addition to schizophrenia. We are extremely excited by the progress made in bringing these diagnostic products to physicians and, most importantly, to the patients that can benefit from them. Unfortunately, there is currently no timeline for the availability of these new products in the United States or any other markets.

If you would like to receive information about our next generation of tests and their availability, please enter your email below. We will use this email distribution to release updates and news about the development of these new tests.

Thank You.”

Note the phrases:

  • in an effort to improve its utility
  • the product needed further refinement
  • there is currently no timeline for the availability of these new products 



Psynova Neurotech, established in 2005 by Sabine Bahn and Chris Lowe, PhD, Director of Cambridge University’s Institute of Biotechnology


AUSTIN, Texas–(BUSINESS WIRE)–Rules-Based Medicine, Inc. (RBM), the leading multiplexed biomarker testing laboratory, announced today that it is partnering with Psynova Neurotech to co-develop and commercialize a blood test for the diagnosis of schizophrenia. RBM and Psynova will focus on the unmet clinical need for an objective and reliable diagnostic test to accelerate and optimize the treatment of schizophrenia. Under the terms of the agreement, the companies will collaborate on the validation, regulatory approval and manufacture of a diagnostic blood test for schizophrenia that will be sold worldwide exclusively by RBM.


May, 2010 Schwarz et al article published in Biomarker Insights journal 


Professor Sabine Bahn, MD, PhD, MRCPsych, Director of the Cambridge Centre for Neuropsychiatric Research (CCNR) and Director/Cofounder of Psynova Neurotech Ltd, presented her research at the APA annual conference in Hawaii (May 14-18)

April 27, 2011 Myriad Genetics announced that it was going to acquire RBM and set up a subsidiary known as Myriad RBM, running it from RBM’s existing premises in Austin

June 23, 2011 According to Business Weekly, Myriad Genetics completed the $80 million cash acquisition of the PsyNova + Rules-Based Medicine company.

August 10, 2011 Michael Spain, MD, Chief Medical Officer of Myriad RBP is quoted in Psychiatric Times as saying that “…psychiatrists in a variety of treatment settings have ordered the test for hundreds of psychiatric patients,” at a cost of $2,500 per test, and that “…numerous insurance carriers…” were paying for it.

January 2, 2013

VeriPsych suspends the test.

So what happened?  What went wrong?  Within psychiatric circles, a valid blood test for the condition known as schizophrenia would be the media equivalent of aliens landing in Times Square.

Unfortunately, everybody concerned, including Fuller Torrey and the Stanley Medical Research Institute are keeping their heads down.  The timing of the sale of PsyNova for $80 million seems significant.  That is an awful lot of money for something that “needs further refinement” and for which no marketing date is available.


I have no inside information as to what went wrong on this study, but here’s a little analogy that might go some way to explaining the matter.

Suppose my wife and I decide to rent out the upstairs of our house, but we particularly don’t want tenants who play loud music.  So we decide to develop a test that will enable us to distinguish these individuals from people who play their music quietly.  We live in a small village, and we decide to conduct our research here.

There are 100 houses in our village, and for simplicity’s sake let’s say that there’s one person living in each house and we have 10 items of information on each person.

So we walk around the entire village every day for, say, a month.  We carry a decibel meter and we take noise measurements at each house.  At the end of a month, we average the daily readings from each premises and then we begin bumping this data against the ten items that we know about each occupant.

Let’s say that one of these items is age, and we find a correlation between age and noise.  The older the occupant is, the lower the decibel number.  But the correlation isn’t all that good.  There are some noisy old folks, and some quiet young people.  So we arbitrarily decide that we’re going to use , say, 20% of a person’s age, as a negative factor on the noise predictor scale.

Another item of information that we have is whether each individual is right or left-handed, and we notice that the left-handed people are far noisier than those who are right-handed.  So we give being left-handed a 60% weighting.  People who are left-handed will get 0.6 (60% of 1) added to their noise-prediction score.  Right-handed people get 0.  And so on for the rest of the information.

Then we add up each person’s scores on the noise prediction scale, and if we’re lucky, all the high scorers will be noisemakers and all the low scorers will be quiet people, and voila, we have a simple way to predict if a prospective tenant will be noisy or quiet.  The string of fractions (60% left-handed – 20% age + … etc) is called an algorithm.

In actual research, however, results are seldom that clear cut.  It is more likely that we will have a scale that discriminates with less than perfect accuracy – say 60%.  So we start to “tweak” the weightings that we assigned to each item of information.  Instead of 60% for left-handedness, perhaps it would be better it if were 65%.  Or perhaps the age score should be weighted at 27%, and so on.  Doing this by hand would be tedious and time-consuming, but with computers one can bump any combination of weightings against the criterion measure with little difficulty.  And in this way, we find the combination of fractions that gives us the most predictive algorithm.

The authors of the study started with 181 blood tests, from which they identified 51 tests that had some correlation with the “schizophrenia” group.  They then ran these 51 tests on 806 participants (577 schizophrenia; 229 controls), and from this data they developed an algorithm that separated the schizophrenia participants from the controls with an 83% accuracy rate.  They report that “…all elements of the data set were used to train the algorithm.”

“Training” the algorithm is what I’ve called tweaking in the example above.  But there’s a problem.  By tweaking the data so thoroughly, what I’ve actually produced is a noise algorithm that may work reasonably well for our village at this point in time.  It might not work in the next village or even in our village next year.  (It may be, for instance, that the high correlation that we found between noisiness and left-handedness is a complete fluke that has no validity outside our village.)  This is particularly pertinent in that noisiness is not some kind of inherent trait like left-handedness or tallness.  Rather it’s a behavior, and behaviors are acquired (or not acquired) through a complex and highly individualized process of interaction between a person and his environment.  Two people who are inherently very different might both score high on a measure of noise, while identical twins might score at opposite ends of the scale.

The general point is that if one is working with a discrete set of data and a fairly large number of variables, it’s usually possible to construct an algorithm that will separate the individuals with a reasonable degree of accuracy along a given criterion.  In other words, if one can tweak the algorithm more or less indefinitely, and add, or drop, variables at will, a pattern will eventually emerge.  The pattern is not necessarily spurious.  It may be a real pattern, but it only applies to the individuals concerned.  I don’t know if this is what happened in the Schwarz et al study, but it might be something along those lines.  All concerned are staying fairly quiet about it.  So perhaps we’ll never know.


Another critical issue in this matter is the nature of the criterion variable and the accuracy with which it can be measured.  In my hypothetical noise study, I have a fairly objective measure (decibels).  But it’s not perfect, because, firstly, I’m taking only one measurement per day, and secondly, I’m taking measurements from the street, and, for this reason, houses that are built closer to the street will, other things being equal, score higher than houses that are set further back.  In the case of the condition known as schizophrenia, the situation is hopelessly confounded because all the DSM items that define the condition are vaguely-defined behaviors, the assessment of which is inevitably subjective.  In other words, if you choose, say, 1,000 people at random and ask 20 psychiatrists to examine all of them and identify and list those who “have schizophrenia,” you will get 20 different lists.  (There will be some overlap, of course, but you will not get perfect concordance.)  So an algorithm that’s been trained on the basis of one of these lists may not work very well on another.

In this regard, there are two interesting quotes from Emily Deans, MD, a Psychiatry Department instructor at Harvard, in the second Psychiatric Times article mentioned earlier.

“Since the diagnoses are based on a recipe list of symptoms from DSM-IV and not known brain pathology, new biologic markers and tests are re-searched and validated against the formal diagnostic criteria.  These criteria are designed to be assessed by mere observation and questioning of the patient.  Thus, biomarkers only end up as valid as the original criteria, or less so, depending on the validation of the scale used in research…” [Emphasis added]


“…biomarkers based on DSM-IV will never be as useful as ground up research to link known brain, gene, and MRS findings to the patient’s symptoms.”

What Dr. Deans is saying here, in effect, is that schizophrenia, as defined by DSM (which is the only way it can be defined) will never be linked reliably to specific neural pathology.  This is something that we “mental illness deniers” have been saying for decades.  Psychiatrists, on the other hand, have been saying, with a level of confidence bordering on recklessness, that schizophrenia (as defined by DSM) is a brain illness, and they even claimed to have identified the neural deficit involved (the now discredited dopamine theory of schizophrenia.).

But it should not be concluded that Dr. Deans or psychiatrists generally are retreating from the bio-psychiatric perspective.  Rather, psychiatry’s position is shifting from the “schizophrenia-is-a-brain-illness” stance of former years to “schizophrenia-is-many-brain-illnesses” which is becoming the rallying cry of the present.  And they’re going to identify each one through ground-up molecular research any decade now.  Meanwhile, by some extraordinary coincidence, neuroleptic drugs are the appropriate “medication” to correct all of these illnesses.  What a stroke of luck!


I was about to publish this post last week, when I ran one last Internet check on VeriPsych to see if there were any updates.  To my surprise, I found a promotional video which was published on YouTube on February 11, 2014.  The video is titled New Blood Test for Schizophrenia.  Here’s a quote from the narrator:

“Researchers…at the University of Cambridge have been working on a blood test for schizophrenia for many years.  A first test was launched in 2010, but later withdrawn from the market, as the price tag of around 2000 Euros was too expensive for wide usage.”

So VeriPsych was withdrawn because it was too expensive.  The earlier announcement on the VeriPsych website (that is still there at the time of this writing) said that it needed “further refinement” in order to “improve its utility.”  So does it need refinement or a price cut?

Another quote:

“They have now developed a new version, which they claim is cheaper, and provides more detailed information for the diagnosis.  The test looks at certain proteins in blood samples of patients to distinguish between different kinds of mental illnesses.  Researchers say that the new test is able to diagnose schizophrenia with a certainty of 83%, and depression with a certainty of about 90%.  Although the test could never stand on its own, it provides doctors and patients with valuable backup information.”

 But the test isn’t quite ready for market yet.

“Sabine Bahn and her colleagues want to launch the new test within this year.”

The video is professionally produced and will probably catch some attention, but there are too many unanswered questions.  Firstly, why was the test pulled if, as reported, it had been selling well and its cost was being reimbursed by insurance companies?  Secondly, if it just needed a price cut, couldn’t this have been done more or less instantly rather than being off the market for 13 months?  Thirdly, is this the same test with the 51 “disease signature” analytes that was described in the original study?  If so, then where did the additional information concerning depression screening with 90% accuracy come from?  If not, has the new test been written up in a peer-reviewed journal?  Fourthly, – and most importantly – what prompted the January 2013 statement that the test “needed further refinement,” if the 2010 beta test had confirmed that “the test worked as intended”?

To me, it just seems like we have too many questions.


Genetic Protection Against Schizophrenia?

On November 12, 2013, Molecular Psychiatry published online Evidence that duplications of 22q11.2 protect against schizophrenia, by Rees et al.  The print version was published last month – January 2014.

Here’s the authors’ summary:

“A number of large, rare copy number variants (CNVs) are deleterious for neurodevelopmental disorders, but large, rare, protective CNVs have not been reported for such phenotypes. Here we show in a CNV analysis of 47 005 individuals, the largest CNV analysis of schizophrenia to date, that large duplications (1.5–3.0 Mb) at 22q11.2—the reciprocal of the well-known, risk-inducing deletion of this locus—are substantially less common in schizophrenia cases than in the general population (0.014% vs. 0.085%, OR=0.17, P=0.00086). 22q11.2 duplications represent the first putative protective mutation for schizophrenia.”

The idea of a genetic mutation that would protect one from schizophrenia aroused a good deal of interest and enthusiasm.

Schizophrenia Research Forum, for instance, ran the headline Protection From Schizophrenia – Too Much 22q11.2 is a Good Thing on an article dated November 22 2013, and Genetic protection Against schizophrenia on another article on the same date.

The Simons Foundation Autism Research Initiative used the headline Duplication of chromosome 22 region thwarts schizophrenia on a January 2, 2014, piece.

The Rees et al paper has added some impetus to psychiatry’s claim that the condition known as schizophrenia is a genetic disease and, for this reason, I thought it might be helpful to take a closer look at the study.

Let’s start by examining what the authors’ summary actually says.

Copy number variants (CNVs) are essentially sections of the DNA string that contain variations from normal.  The DNA is the “blueprint” of the organism, so variations in the string always have the potential to cause variations in the structure of the organism.

There are two kinds of CNVs: deletions and duplications.  In deletions, a small piece of the normal code is omitted; in duplications, a piece is inserted twice.

When the authors write that a number of CNVs are deleterious for neurodevelopmental disorders, what they mean is that there is an association between having the CNV and having the disorder.    Rees et al focused on the part of the genome designated 22q11.2: a small section near the middle of chromosome 22.


Deletions in the 22q11.2 area are associated with numerous features, ranging both in number and severity.  These features include:  heart disease; palate abnormalities; unusual facial features; learning difficulties; renal abnormalities; hearing loss; autoimmune illnesses; etc…  22q11.2 deletions are also associated with autism and low IQ in childhood, and with “schizophrenia” in later years.  The condition is called DiGeorge syndrome.

About 5% of 22q11.2 deletion syndrome cases are inherited.  The remaining are new mutations, and arise because this DNA region is vulnerable to rearrangement when sperm and ovum cells are being formed.  The precise mechanism by which 22q11.2 deletions cause the various birth defects mentioned above is unknown, but is believed to involve structural anomalies in the embryonic pharyngeal area, which in turn cause defects in the thymus and parathyroid glands.


Duplications on 22q11.2 are associated with low IQ, learning problems, psychomotor delays, and growth retardation.  The mechanism by which the duplications produce these problems is unknown.

In addition, duplications on 22q11.2 can be inherited from a parent whose development has been normal, so there is not a clear one-to-one relationship between the syndrome and the genetic duplication.


The Rees et al study searched for 22q11.2 duplications in a sample of 6,882 individuals who had a “diagnosis of schizophrenia,” and in another group of 11,225 individuals drawn from four non-psychiatric data sets.

Their results are summarized in the table below:

Schizophrenia Controls
Duplication 0 10
No duplication 6,882 11,245
Total 6,882 11,255


On the face of it, this result looks impressive.  Of the 6,882 cases with a “diagnosis” of schizophrenia, there were none that had a duplication on 22q11.2.  And so it might be argued, and indeed is being argued, that the genetic duplication in question protects  one from becoming schizophrenic.

However, if we look at the right side of the table, we see that only 10 individuals out of the 11,255 controls actually had the duplication.  So even if we assume that the study is methodologically sound, and that schizophrenia vs. non-schizophrenia is a valid dichotomy (which, incidentally, it isn’t), it is clear that only a tiny fraction (less than 1 in 1000) of the controls owe their “illness-free” status to 22q11.2 duplication.

This can be seen more readily if the data is viewed diagrammatically as below.  The areas of the circles represent the sizes of the three groups:  those with “schizophrenia” (blue);  the controls (orange); and those with the genetic duplication (white).  All of the latter group fall within the controls’ circle, but are still a tiny part of that group.

First Circles2

Incidentally, Rees et al report that their result is statistically significant (p = 0.017).  What this means is that the way the ten people with duplications are distributed (i.e. 10 in the control group and none in the “schizophrenic” group) has only a 1.7% chance of being a random fluctuation.  In other words, it is probably a genuine skew.  But it is also a very small effect.  The statistical significance of a result is largely a function of the sample size, and is not indicative of the magnitude of the effect.  On the basis of this study, for instance, one could tentatively conclude that there is an association between having the genetic duplication and not having a “diagnosis” of schizophrenia, but that the association is very weak.  The putative protection factor applies to fewer than one person in a thousand.

Rees et al continued their study by obtaining and combining more cases from other CNV data sets.  They obtained 22q11.2 duplication data on an additional 14,256 “schizophrenia” cases and 14,612 controls.  They found essentially the same association, but again the association was weak.

Schizophrenia Controls
Duplication 3 12
No duplication 14,253 14,600
Total 14,256 14,612


Or expressed diagramatically:

Second circles2e

[Note:  In this diagram, a small segment (3/15) of the duplication circle should be in the blue circle, but MS Word draw function wouldn’t cooperate.  Or perhaps I wasn’t cooperating with MS Word?]

Next the authors combined the two sets of data to produce the following overall result:

Schizophrenia Controls
Duplication 3 22
No duplication 21,135 25,845
Total 21,138 25,867



Third cirles

[Note: Again, a small section of the duplication circle should be in the “schizophrenic” region.]


Perhaps the most obvious point that needs to be made is that the DNA is the organism’s blueprint, and as such it determines how the organism will be formed (two eyes, two hands, one heart, etc.); the spatial arrangement of these parts; and the material (bone, muscle fiber, etc.) from which these parts will be made.  The DNA determines the organism’s structure.

Links between the DNA and the organism’s activities are always mediated by one or more intervening factors.  This is important in the present context because the condition known as schizophrenia is – by definition – a cluster of activities in which the person engages.

To illustrate this, let’s consider polycystic kidney disease (PKD).  This is a good example, because it is a clear-cut genetic illness caused by cysts in the kidneys.  The cysts block the flow of blood through the kidneys, and, as the cysts proliferate and grow larger, the kidneys are destroyed.

The cysts are caused by a defective gene.  (Actually there are two, possibly three, genes that can produce PKD, but about 80% of cases arise from the gene PKD-1, and for the sake of simplicity, we’ll confine our attention to that.)  A gene, incidentally, is a piece of the DNA string – a piece of the organism’s blueprint.  In polycystic kidney disease, the PKD-1 gene conveys faulty instructions concerning the walls of the tiny tubes (nephrons) in the kidneys.  Instead of calling for ordinary nephron epithelium in these locations, PKD-1 calls for cyst wall epithelium.  And cyst wall epithelium produces fluid which accumulates in, and ultimately destroys, the nephrons and the kidney.

So the gene determines the structure of the nephron wall.  This structure in turn causes the cyst wall epithelium to produce fluid.  This activity is a direct effect of the structure.  Secondly, as the nephrons become increasingly blocked, the kidneys produce less urine.  So, reduced urination is a secondary functional effect of the gene PKD-1.  Thirdly, a child growing up with polycystic kidney disease is, other things being equal, likely to feel sick and under-the-weather much of the time, particularly if the disease has not been recognized and remedial/palliative measures have not been taken.  Such a child, again other things being equal, is likely to be fussier and more tearful than other children, and it is entirely possible that one could find a weak correlational link between gene PKD-1 and childhood fussiness, though, of course, any search for such a correlation will be confounded by the obvious fact that children can be habitually fussy for other reasons.

And from there the causal chain could continue in various ever-weakening directions.  For instance, the child might become somewhat sad and despondent.  Or it could be that the child received extra attention and comforting from his parents and was fairly content, and so on.  Ultimately the outcome is impossible to predict with any kind of precision, and the best we can expect from genes vs. subsequent behavior studies are weak, tenuous correlations.

With regards to the very weak inverse link between 22q11.2 duplication and the condition known as schizophrenia, we can barely speculate as to the nature of the casual sequence, because it is not known how 22q11.2 duplication expresses itself in the organism structurally.  The authors state that 22q11.2 duplication is positively associated in children “…with a wide range of psychiatric and behavioral abnormalities…including attention deficit hyperactivity disorder and autism, as well as other social and behavioral problems,” and they cite various references in support of this statement.  So what we’re left with from Rees et al is that 22q11.2 duplication is positively associated with low IQ and with various psychiatric and behavioral problems in childhood, but, by contrast, is negatively associated with a “diagnosis” of schizophrenia in adulthood.

A “diagnosis” of schizophrenia hinges on complex social activities that arise relatively late in life, and cannot be direct effects of a genetic anomaly, or even several anomalies.  To illustrate this, let’s go back to the 22q11.2 deletions discussed earlier.  I mentioned that deletions in this DNA segment are associated with various problems, including palate abnormalities.  The palate abnormalities are a direct effect of the gene defect.  One of the palate abnormalities associated with these deletions is cleft palate.  This condition, if not corrected surgically, results in a characteristically strained and nasal speech quality, which in severe cases can be quite stigmatizing.

The cleft palate is a direct effect of the deletion; the nasal speech is a secondary effect of the deletion.

Children with this kind of speech are sometimes mocked and bullied by their peers.  The child might react to this kind of stigmatizing by becoming violent, or by withdrawing socially, or by speaking as little as possible, or in various other ways.  These reactions would be considered tertiary effects of the deletion.  And so on.  Each step in the chain takes us further from the genetic anomaly, and the statistical associations grow commensurately weaker.  In the case of a child who became violent in response to the taunting, it would be stretching the matter to say that the violence was caused by 22q11.2 deletions.  Nor would one conclude that the child’s violent acts were symptoms of a genetic disease.  In fact, conceptualizing the child’s violence or social withdrawal as a symptom of 22q11.2 deletion would generally be considered nonsensical.  And this is true even though the link between the deletion  and the cleft palate is clear-cut and direct.

In the same way, it is simply not tenable to claim that “schizophrenic” behaviors (e.g. disorganized speech) are symptoms of a genetic disease.  This is particularly the case in that correlations between the diagnosis and genetic anomalies are typically very small, and the so-called illness doesn’t usually emerge until age 20 or later.  The effects of any genetic anomalies that might be correlated have had ample opportunity to be modified and shaped by social and environmental factors, and in the absence of a clear and readily understandable link between the “symptom” and a genetic defect, the social and environmental factors are more credible causal constructs.

“Schizophrenia” is not a unified condition.  Rather, it is a loose collection of vaguely defined behaviors.  For this reason, any genetic research done on this condition will inevitably result in conflicting and confusing results.  It’s like looking for genetic similarities in all the people who play scrabble, or cheat on their taxes, or collect postage stamps, or whatever.  If the sample sizes are large enough, one could probably find small effects in all or most of these areas, but no one would conclude from this that these are genetically determined activities.

A person’s ability to learn depends on two general factors:  a) the structure of his brain, as determined by his DNA, and b) his experiences since birth.

One can’t learn to play the guitar, for instance, unless one has adequate neural apparatus, and fingers, both of which require appropriate DNA coding.  But even though a person’s genetic endowment might be excellent in these regards, he will never learn to play unless he is exposed to certain environmental factors.  In the same way, a person whose genetic endowment was fairly marginal might become an excellent guitarist with the correct environmental encouragement and support.

Similar reasoning can be applied to the behavior of not-being-“schizophrenic.”  This behavior involves navigating the pitfalls of late adolescence/early adulthood with a modicum of success, and establishing functional habits in nutritional, interpersonal, occupational, and other important life areas.  Clearly it requires adequate neural apparatus, hence the weak correlations with genetic material, but equally clearly it requires an appropriately nurturing childhood environment, with opportunities for emotional growth and skill acquisition.

Given all of this, it’s not surprising that researchers are finding correlations between DNA variations and a “diagnosis” of schizophrenia, but given the number of links in the causal chain and the multiplicity of possible pathways at each link, it is also not surprising that the correlations are always found to be weak.

It is not my purpose to disparage genetic research.  In my view it is an extraordinarily promising field that holds the potential to find causes and cures for various illnesses.  In the behavioral field, however, it is being overemphasized at the expense of less dramatic, but ultimately more promising socio-behavioral work.  Looking for the genetic causes of behavioral/emotional problems is a bit like studying the blueprint of a car in an attempt to discover why there is a dent in the fender.  This is a particularly apt analogy, in that if one studied a very large number of dents in different vehicles, one would probably discover a weak correlation between the depth of the dent and the thickness of the steel used in the car’s manufacture.  And this thickness would, of course, be shown on the car’s blueprint.  So there will be a small correlation between an entry on the blueprint and the size of the dent, and this is analogous to the small correlations found between genes and subsequent behavioral problems.

But if we truly want to know why there is a dent in the car’s fender, it might be more fruitful to simply ask the owner.

Schizophrenia Research

Psychiatric News is the APA’s online bulletin.  On Jan 15, it ran an article by Vabren Watts (an APA staff writer).  The article is called APA Gives Schizophrenia Research Capitol Hill Spotlight.

It is reported in the article that on December 12, 2013, the APA, together with the Congressional Neuroscience Caucus and the American Brain Coalition, made a joint presentation to legislators and their staffs on

“…latest research on treatments for schizophrenia…”

The session was moderated by Saul Levin, MD, MPA, who is the APA’s Medical Director and CEO.

APA’s President, Jeffrey Lieberman, MD, participated in the discussion, and reportedly stressed the strong link between psychiatry and neuroscience, and how this

“…may lead to the development of diagnostic tests to help predict the likelihood of schizophrenia episodes in those at greatest risk.” [Emphasis added]

The article is standard psychiatric PR, and the legislators were assured that the APA will continue to be a

“…strong advocate for more federal investment in biomedical research…”

This plaintive cry for government dollars is a constant theme with organized psychiatry.  It has increased in recent years as big pharma, psychiatry’s previous bankroller, is distancing itself, largely for financial reasons, from psychiatry’s trail of destruction and scandal.

But there are two points in the article that, in my opinion, warrant further examination.  They were both quotes from Lisa Dixon, MD, a psychiatrist at Columbia University and the NY State Psychiatric Institute.  Dr. Dixon is also involved in the NIMH-funded RAISE study (Recovery After an Initial Schizophrenic Episode).

Here’s the first quote:

“‘Support for employment and education [for teenagers with schizophrenia] is not something that we typically have in the mental health package. It is critically important to keep these young people in their lives—keeping them on track and on trajectory…'”

There’s some interesting history here.

Prior to the 1980’s, most people with developmental disabilities were either not employed, or were employed in sheltered workshops.  Then the notion that these individuals could, in many cases, obtain and hold down mainstream jobs began to gain currency.  Case managers, trainers, and job coaches throughout the US became empowered to reject the stigmatizing labels of helplessness and dependency that had constituted orthodox thinking concerning these individuals, and today one can find developmentally disabled people working in fast-food restaurants, grocery stores, motels, and other sites.

As the success of these programs became increasingly evident, attempts were made by program managers and staff to provide similar services to people with “mental illnesses,” including “schizophrenia.”  These attempts were routinely resisted by psychiatry, who insisted that because schizophrenia is an incurable, degenerative brain disease, the best we can offer these clients is neuroleptic drugs, forced if necessary, to keep their “illness” in remission, trips to the state hospital for “stabilization” as needed, and a completely non-demanding, unstressed milieu.  Clubhouses and drop-in centers were about as much as they could be expected to handle.

In this historical context, Dr. Dixon’s proclaimed enthusiasm for “keeping them on track and on trajectory” rings a little hollow.  It was psychiatrists, Kraepelinian blinkers firmly in place, that relegated these individuals to the psychiatric wards and the “day treatment” centers and the clubhouses.  It was psychiatrists who told family members, in no uncertain terms, that these individuals were not to be challenged or stressed in any way.  It was psychiatrists who insisted that these individuals would never be able to continue their studies or even hope to hold down jobs.

And all this despite the fact that in pre-Kraepelinian times, individuals with essentially the same presentation were being successfully encouraged to learn new skills, to resolve their problems, and obtain gainful employment.

Psychiatry’s scandalous message of disempowerment, and their routine destruction of these people’s brains with toxic drugs, was not based on any kind of scientific discovery.  Rather, it was based on a slavish adherence to bio-psychiatric orthodoxy; a narcissistic faith in its own pronouncements; and an inexplicable, but apparently endless willingness to inflict destructive “treatments” on those entrusted to their care.

And now – with their concepts debunked, their destructive practices exposed, and their profession reeling drunkenly from one scandal to the next, psychiatry is trying to co-opt the recovery movement with its “discovery” that people with “schizophrenia” need to be kept “on track and on trajectory.”

But there isn’t even a hint of recognition or acknowledgement that it was psychiatry’s condescending dogmatism that knocked these individuals off track in the first place, and that for a hundred years condemned them to a life of disempowerment, hopelessness, horrific “treatments,” devastating adverse effects, and an early death.

The second quote from Dr. Dixon is also in reference to the RAISE study.  She is quoted as saying that the RAISE initiative is not a project in which people seek out the program for support; instead:

“…the program goes to the people.”

In the NIH August 2011 document describing the Columbia RAISE study it states that the project

“…will identify ways to effectively integrate a comprehensive early intervention program for schizophrenia and related disorders into existing medical care systems…” [Emphasis added]

There it is again – a psychiatrist or a psychiatrist’s assistant in every GP’s office, and screening for early intervention.  So a socially awkward teenager, who visits his/her GP for a sore throat, can be shunted across the hall to the psychiatric specialist for “screening.”  The program goes to the people!

And this, coupled with the fact that “attenuated psychosis syndrome” is included in the DSM-5 (p 122), despite APA’s assurances that it would not be, is a cause for major concern.

Despite everything that has been said and written about psychiatry’s spuriousness and destructiveness; despite the outspoken protests of its victims; despite the growing dissent in its own ranks; the psychiatric juggernaut is still at full throttle, expanding its insatiable “diagnostic” net, and selling more drugs to more people.

We can only hope that our legislators have enough sense to see through this self-serving promotion, and start diverting some of these research funds to questions that genuinely need to be addressed.  For instance:  are psychiatric drugs playing a causative role in the mass shootings that have become commonplace in the US in the past 20 years?

Role of Childhood Abuse in Development of “Schizophrenia”


There has been some discussion in recent weeks concerning the role of childhood abuse in the etiology of the condition known as schizophrenia.

It is particularly difficult to address this problem because the condition known as schizophrenia is not a unified phenomenon.  Rather, it is an assortment of loosely clustered behaviors which has been falsely and illogically labeled by the APA as an illness, existing in an individual.

So the question “Is schizophrenia caused by childhood abuse?” is a meaningless question. In other words, it cannot be answered either as “true” or “false.”  In fact, it can’t even be answered “maybe.”

So let’s instead focus on one key aspect of this assortment of loosely clustered behaviors, i.e. delusions.  And let’s rephrase the question:  are delusions in adulthood caused by childhood abuse?

The APA defines delusions as follows:

“A false belief based on incorrect inference about external reality that is firmly sustained despite what almost everyone else believes and despite what constitutes incontrovertible and obvious proof or evidence to the contrary.”  (DSM-IV-TR, p 821)

There are problems with this definition, of course, because one man’s proof is another man’s conspiracy theory.  In other words, the definition presumes that there exists a body of knowledge that is the Truth, which I suggest is a little naïve.

But instead of struggling with these abstruse issues, let’s instead take an example.  Let’s consider the case of a person who believes firmly that the government is spying on him and has tapped his phone, and let’s, for the sake of argument, assume that this contention is false and patently unwarranted.

So the question becomes:  is this belief caused by childhood abuse?  But here again, even in asking this question, we’ve made another unwarranted assumption.  We’ve assumed that believing (without reason) that the government is spying on one is a unified phenomenon which can be attributed to a single cause in all or even most cases.  It’s easy to fall into this trap because science routinely does identify unified phenomena that do indeed admit of a single explanation.  Rainbows, for instance, are caused by droplets of water suspended in the air, together with a certain geometric arrangement of the sun and the observer.  But believing that the government is spying on one (or more correctly expressing the belief that the government is spying on one) is not the same kind of thing.  There are likely to be many reasons why a person would express this belief, and the only way to establish the actual cause in a given individual is to get to know that person and his history, to listen very carefully and empathically to what he has to say, and to try to see the world from his perspective.

Based on my experience, here are some of the factors that might have a bearing on the development of this belief:

1. One’s parent(s) expressed beliefs of this sort and passed them on through normal parent-child interactions.
2.  One has experienced a profound and persistent sense of failure in childhood and early adulthood.
3.  One belongs to a group where the expression of these kinds of beliefs is encouraged and reinforced.
4.  One is copying the views of another person.
5.  One is using, or withdrawing from, certain drugs (including pharmaceutical products).
6.  One has something wrong with one’s brain.  Definite information in this area is hard to find.  But just as hearts, livers, kidneys, etc., can develop problems, brains can also malfunction, and it’s possible that certain malfunctions could precipitate paranoid beliefs.  In my view this factor is extremely rare.

In my clinical experience, the second item above – a profound and persistent sense of failure – is the factor most often encountered in practice; a notion, incidentally, which was propounded by the eminent psychiatrist Eugen Bleuler in 1912.  (Affectivity, Suggestibility, Paranoia, p 97-98)

But here again, the level of individual variation is enormous.  If we pose the question:  why do some people experience so much failure? Numerous scenarios come to mind.  For instance:

1.  Parental expectations were too high given the individual’s general ability.
2.  Basic social skills were not coached (for a variety of reasons).
3.  Parents (or other caregivers) were preoccupied with other matters (e.g. economic survival).
4.  Basic problem-solving and competency skills were not coached.
5.  Child was bullied at school and failed to learn.
6.  Deaths or other tragedies at an early age interfered with skill acquisition.
7.  Parents were poor problem-solvers and failed to pass on the notion that problems are something to be tackled and resolved.
8.  A history of abuse (physical, sexual, or emotional).  To state the obvious, a child who is being abused tends to be preoccupied with matters of survival.  In such a context, skill acquisition often takes a backseat.
9.  Etc., etc., etc…

In other words, there are lots of reasons why a person might experience profound and persistent failure, and some of these individuals will develop paranoid beliefs.  Some of these individuals also have a history of abuse.

There is a strong statistical correlation between acquiring a “diagnosis of schizophrenia” and having a history of abuse (at least 50% in women), and in my view, the possibility of a history of abuse always warrants exploration when working with individuals who express paranoid or otherwise delusional beliefs.

If (when?) the medical model domination of the research agenda wanes, and more psychosocial research is pursued, I believe we will see increasing evidence for this position.

What I have tried to do in this post is put the abuse question into perspective.  Similar analyses could be done on the other “symptoms” of “schizophrenia.”

The central point I’m making is that people are complicated.  We are each a bewildering tapestry of threads drawn from different sources, dyed in different vats, and interwoven in an endless and ever-shifting array of circumstances and conditions.  There are no simple, pat explanations of any human activity, including expressing paranoid beliefs.  The only way to gain any significant insights into these kinds of matters is to take the time to get to know the individual, to establish trust, and to form a constructive alliance.  There are no shortcuts.

Talk Therapy for Schizophrenia

There’s an interesting article on Vermont’s Seven Days.  It’s called Burlington’s HowardCenter Tries a New Approach to Treating Mental Illness: More Talk, Fewer Meds.  You can see it here.  (Thanks to Steven Coles on Twitter for the link.)

Apparently Vermont’s Department of Mental Health is promoting a “new” kind of treatment for psychosis:  talk therapy.  The project leader is Dr. Sandra Steingard, who for most of her career accepted the orthodox view of schizophrenia and the need for neuroleptic drugs.

But then an interesting thing happened.  She read Robert Whitaker’s book Anatomy of an Epidemic.  One of the highlights of Robert’s book was the notion that the loss of brain tissue, which psychiatry had long insisted was a consequence of schizophrenia, was actually caused by the neuroleptic drugs.

Dr. Steingard says that reading this was like being “kicked in the belly.”

“If you’ve just spent your entire career giving people these drugs, and in many cases convincing people why this is what they really need to do, that’s a pretty horrible thing,” she says. “I wasn’t sure I would come to work the next day. That’s how profound it was.”

The Vermont program is called Open Dialogue.  Psychologist Greg Tomasulo is the Clinical Director.  He is quoted as saying:

“One way of thinking about schizophrenia is that it’s a brain disease… Another is that it’s how somebody expresses their most difficult experiences in a way that they can’t yet put into words, so they use hallucinations and delusions to express themselves.”

“By learning other ways of talking about difficult experiences,” he adds, “the patient no longer needs those symptoms anymore and they ‘resolve.'”

It sounds like a good program, and it will be interesting to watch its development.  It will also be interesting to see if there are attempts by mainstream psychiatry/pharma to marginalize or discredit the program.

“You must take these pills for life.” Or is it for death?

There’s an important article (here) on Monica Cassani’s website BeyondMeds in which she tackles the myth that once a person has been assigned a “diagnosis” of schizophrenia, he/she must take neuroleptics for life.

Here’s a quote:

“Unfortunately, at this juncture in history many people who get labeled with psychiatric illness these days do not have the opportunity for recovery because they are encouraged to stay ill by a system that all too often impedes psychological growth by use of excessive psychotropic drugs. This over-use of medication also kills people. The average life-span of people taking these medications is 25 years shorter than people who do not take these drugs. The drugs cause a long laundry list of problems only some of which are diabetes, obesity, heart conditions and a shrinking brain.”

Given the devastating effects of neuroleptic drugs, including premature death, the schizophrenia falsehood is arguably the most damaging facet of modern psychiatry.

Please check out the article and pass it on.

Neuroleptics Increase the Risk of Osteoporosis

We’ve all known for a long time that neuroleptic drugs damage brain cells.  But now it seems clear that they also increase the risk of osteoporosis and consequently bone fractures.

There’s an article about this in the International Journal of Endocrinology, dated March 2013.  It’s titled Osteoporosis Associated with Antipsychotic Treatment in Schizophrenia, and was written by Haishan Wu et al, from the Central South University in Changsha, China.  I came upon the article through Robert Whitaker’s site Mad in America.

The paper is a study review and cites 68 references.  The authors conclude that there are extensive indications:

“…that osteoporosis is associated with schizophrenia particularly in patients under psychotropic medication therapy. As osteoporotic fractures cause significantly increased morbidity and mortality, it is quite necessary to raise the awareness and understanding of the impact of antipsychotic induced hyperprolactinemia on physical health in schizophrenia.”

They also point out that:

“Antipsychotics are the most common cause of pharmacologic hyperprolactinemia, and the majority of antipsychotic agents cause hyperprolactinemia.”

In addition, they outline the mechanism by which neuroleptic drugs promote hyperprolactinemia, and how this in turn leads to osteoporosis and increased risk of fractures.

The authors point out that hyperprolactinemia has other adverse effects, including galoctorrhea (spontaneous flow of milk from the breast, unassociated with childbirth or nursing), amenorrhea, absent ovulation, sexual dysfunction, and cardiovascular disease.

From some of the papers cited in this report, it is clear that the causal link between neuroleptics and reduced bone density has been documented since at least 1987 (T. Higuchi, T. Komoda, M. Sugishita et al., “Certain neuroleptics reduce bone mineralization in schizophrenic patients,” Neuropsychobiology, vol. 18, no. 4, pp. 185–188, 1987).

How often do you suppose there has been genuinely informed consent in the prescription of these drugs?