Tag Archives: schizophrenia

More on the Biological Evidence for “Mental Illness”

On January 10, 2017, I put up a post titled The Biological Evidence for “Mental Illness”.  It was published simultaneously on Mad in America.  The post was a response to an earlier comment from Carolina Partners in Mental Healthcare PLLC, which included the assertion “mental illnesses have a long history of biological evidence.”  In my January 10 article, I challenged this assertion and pointed out that no such evidence existed.  The article generated some comments, most of which were favorable.  There was one comment, however, from Michael, who asserted:

“Your rebuttal that there are no scientific studies to these cases can be dismissed with a quick google search.”

In my response to Michael, I asked him to cite me some references to support this assertion.  On  January 15, Michael wrote back citing three studies:  the first on the neurobiology of depression; the second on the neurobiology of “schizophrenia”; and the third on the neurobiology of “bipolar disorder”.

I examined these studies, and started to draft a response to Michael, but as I was writing, I realized that the subject matter warranted a wider audience and needed to be put up as a post.  This is not because the studies cited are particularly compelling.  As we shall see below, they are not. But rather, because what has happened here is something that occurs routinely in these debates.  Psychiatry proponents claim there is evidence to support their position that “mental illnesses” are caused by biological malfunctions – but when pressed for references, they either don’t respond at all, or they dish up the kind of references cited by Michael.

All three papers are literature reviews.


Maletic V, Robinson M, et al, Neurobiology of depression: an integrated view of key findings, Int J Clin Pract, 2007 Dec; 61(12): 2030–2040.

From the point of view of Carolina Partners and  Michael’s original assertion, this study is particularly easy to rebut.  In fact, the authors do it for us.  Here’s the conclusion:

“Major depressive disorder is an illness with significant neurobiological consequences involving structural, functional and molecular alterations in several areas of the brain. Antidepressant pharmacotherapy is associated with restoration of the underlying physiology. Clinicians are advised to intervene with MDD using an early, comprehensive treatment approach that has remission as the goal.” [Emphasis added]

Note that the authors are stating clearly that the structural, functional, and molecular neurobiological alterations are consequences of depression, not causes.

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

But the article has many additional points of interest.  Here are some quotes:

“Although much information still needs to be attained, imaging and other methods have begun to elucidate the neurobiological abnormalities associated with MDD. In particular, several prefrontal and limbic structures and their interconnected circuits have been implicated in affective regulation (Figure 2). These neuroanatomical areas include the ventromedial prefrontal cortex (VMPFC), lateral orbital prefrontal cortex (LOPFC), dorsolateral prefrontal cortex (DLPFC), anterior cingulated cortex (ACC), ventral striatum (including nucleus accumbens), amygdala and the hippocampus. Abnormalities in these areas have been shown in patients with MDD compared with healthy controls and thus suggest a foundation for the symptomatic expression of MDD (24, 25). However, these deviations may be obscured or not present at the individual patient level and thus, these findings cannot necessarily be considered pathognomonic.” [Emphasis added]

Note the admissions that:

“…much information still needs to be attained…”
“…imaging and other methods have begun to elucidate…” [Emphasis added]
“…implicated in affective regular…” [implicated in is not synonymous with causative of]
“…suggest a foundation…” [Emphasis added]
“…deviations may be obscured or not present at the individual patient level…” [Emphasis added]

This doesn’t sound very definitive or convincing.

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

“Combining the evidence from these genetic, cross-sectional, and clinical treatment studies suggests that morphological differences in the hippocampus may be a predisposing factor in MDD, but changes can also accumulate in the course of the disease and thereby create an obstacle to full recovery.”

Again, note the vagueness:

“Combining the evidence…suggests…” [Emphasis added]
“…differences in the hippocampus may…” [Emphasis added]
“…be a predisposing factor in MDD…”

The ever-present predisposing factor – not quite the same thing as a cause – but good enough to convey the impression of causality.

But look at the last phrase in the quote:

“…changes can also accumulate in the course of the disease and thereby create an obstacle to full recovery.”

What the authors are suggesting here is that depression  causes neurological pathology “in the course of the diseases” and that this pathology could create an obstacle to full recovery.  Of course the drugs and hi-voltage electric shocks to the brain that psychiatrists routinely use to “treat” depression also cause neurological pathology.

And lest it be feared that I’m cherry-picking quotes that are particularly vague and unconvincing, the word “may” occurs 21 times in the paper, e.g. “this abnormal activity pattern may be responsible for the manifestations of symptoms associated with MDD”; “Symptomatically, disruptions as a result of proinflammatory cytokines may be experienced as fatigue, loss of appetite and libido as well as hypersensitivity to pain.”  The word “could” occurs three times and the word “suggest(s)” ten times.

Here’s the final sentence of the study:

“Once remission is attained, maintenance of effect may become the more appropriate term, rather than relapse prevention, to emphasise the necessity for an ongoing collaboration between patient and physician in order to maintain neurobiological homeostasis.”

And what do you think is going to happen in this “…ongoing collaboration between patient and physician…”?

Here’s a clue:

Vladimir Maletic has served on the Speaker’s Bureau or has been a consultant for Eli Lilly and Company and Cephalon.  He did not receive any financial compensation for his work on this manuscript. His co-authors are each employees and/or shareholders of Eli Lilly and Company”

And incidentally, according to Dollars for Docs, Dr. Maletic received $841,342 from pharmaceutical companies between August 2013 and December 2015.  In 2015 alone, he received 460 payments from pharma companies for a range of activities including promotional speaking, honoraria, consulting, education, food and lodging, etc.  According to his biography on Global Medical Education, he is a Professor of Neuropsychiatry and Behavioral Science at the University of South Carolina School of Medicine.


Ross CA, Margolis RL, et al, Neurobiology of Schizophrenia,  Neuron, October 5, 2006, 52, 139–153

Here again, the authors themselves have provided the rebuttal of Michael’s assertion.  The final section of the paper is Conclusions and Possibilities for Future Research.  Here are the first two sentences.

“In conclusion, we now believe that the molecular genetics of schizophrenia are sufficiently advanced such that etiology-based studies of the neurobiology of schizophrenia are both justified and feasible. The field is still in its infancy, and we must struggle to integrate our rudimentary knowledge of schizophrenia genetics with our scarcely better developed understanding of normal human brain function.”

So, etiology-based studies of the neurobiology of “schizophrenia” are justified and feasible.  Which, of course, is a clear admission that the evidence is not to hand.

Later in the same section there’s this gem:

“The genes associated with schizophrenia may have a spectrum of different pathogenic effects, altering neuronal development, neuronal plasticity, and signal transduction. While undoubtedly a great oversimplification, it may be of heuristic value to postulate that variations in particular genes can affect particular neurobiological processes (Figure 6), in turn causing specific phenotypes.” [Emphasis added]

So the genes associated with “schizophrenia” may have a spectrum of different pathogenic effects.  This is very vague.  The use of the word “may” clearly implies that they also may not have such effects.  But in any event, the evidence for such effects is not adduced in the paper.

And the assertion “…it may be of heuristic value to postulate that variations in particular genes can affect particular neurobiological processes…in turn causing specific phenotypes”, simply means that the hypothesis that genetic variations affect neurobiological processes, which in turn cause psychiatric “symptoms” may have value in encouraging us to explore and learn, which isn’t particularly profound.  Any hypothesis can act as a stimulus to explore and learn.

Here are three more quotes from the section headed Neuropathology:

“Neuropathological investigations of schizophrenia…have not found any evidence of the usual features of neurodegenerative diseases, such as inclusion bodies, dystrophic neuritis, or reactive gliosis.  There is intriguing, though not always consistent, evidence of subtle cytoarchitectural anomalies in entorhinal gray matter…and in other corticolimbic regions, and an abnormally high frequency of aberrant neurons in the white matter underlying prefrontal cortex…temporal, and parahippocampal regions…While these findings remain open to various interpretations…together they provide suggestive evidence for subtle abnormalities in neurodevelopment in schizophrenia, such as disordered cortical neuronal migration, consistent with the observation of subtle behavioral, neurological, and morphologic abnormalities.” [Emphasis added]

“Gene expression array studies have compared the expression profiles, in a number of different brain regions, of schizophrenias and controls…These studies have yielded inconsistent results and still need to overcome the difficulties inherent in the usage of postmortem brain tissue.” [Emphasis added]

“These studies may allow us to reconceptualize our definitions of the psychiatric disorders, including schizophrenia, based on a better understanding of etiology and pathogenesis.”

They may indeed – but clearly the authors are not saying that the evidence is in.  In fact, in the Introduction to the article, they stated that:

“We argue in this review that a definitive study of the neurobiology of schizophrenia is now possible.”

The definitive study is “now possible”!  This paper is dated October 2006, more than ten years ago.  Why haven’t we seen the definitive study yet?  Could it be, could it possibly be, that psychiatry, driven by its own self-centered considerations, is barking up the wrong tree?

Under the ACKNOWLEDGEMENT heading, the paper states:

“NARSAD, Stanley Medical research institute, NIMH, NINDS, and Johns Hopkins Psychiatry provided support.”


The word suggests(s) occurs 26 times; may, 57 times; can, 28 times; might twice; and could seven times.


Muneer A, The Neurobiology of Bipolar Disorder: An Integrated Approach, Chonnam Med J., 2016 Jan; 52(1):18-37

Once again, let’s start with the author’s own assessment of his paper.  The Conclusion section begins:

“A broad assessment of the current literature was done to bring to light the underpinnings of mood disorders in general and BD in particular. These are stress-related conditions with overt expression in individuals with an underlying genetic vulnerability. Modern neuroscience is utilizing animal models and conducting human research with increasingly sophisticated methods to unravel their pathophysiology. Significant strides have been made in understanding the neurobiology of affective illnesses, and in this regard new targets and biomarkers have been identified. Diverse biological systems act in concert in perpetuating the disorders. While obstacles in research remain in the basic scientific and clinical domains, there is no doubt that a representation is emerging that is providing a consolidated view regarding the development of these intractable conditions. It is hoped that new knowledge will translate into novel therapeutic measures that have both preventive and curative value for patients with bipolar spectrum disorders.”


“Modern neuroscience is [working]… to unravel their pathophysiology.”  The clear implication is that they haven’t unraveled it yet.

“Significant strides have been made in understanding the neurobiology of affective illnesses,”.  This is not what researchers say when they’ve made the great discovery.  They say Eureka!

“… new targets and biomarkers have been identified.”

Biomarkers sounds pretty good.  After all, it is widely claimed by psychiatry proponents that the identification of the elusive biomarkers is just around the corner.  It is widely promoted that the biomarkers, when discovered, will clinch the biological pathology issue once and for all.  So is that what the author is saying here?  Well, no.

It is clear from the text that what this author means by “biomarkers” is simply a biological factor that correlates to varying degrees with the bipolar label.  The author presents a few examples, but for illustrative purposes, let’s examine just one:  cortisol levels in the blood stream.

“Early in the trajectory of BD, episodes occur secondary to stress but there is blighted psychobiological resilience and defective coping that increase vulnerability to recurrent affective exacerbations with illness advancement.12  This impairment is principally provoked by the hypothalamic-pituitary-adrenal (HPA) axis, which does not function properly in patients with BD.13 Patients with BD have a hyperactive HPA axis, high levels of systemic cortisol, and nonsuppression of its circulating levels in the dexamethasone suppression test or the dexamethasone/corticotrophin-releasing hormone (DEX/CRF) test.14

This is a bit technical, but here’s the translation:

  1. In the early stages of those behaviors, thoughts, and feelings that psychiatrists label bipolar disorder, episodes of mania and depression occur in response to stress.
  1. But, as more episodes occur, there also occurs blighted psychobiological resilience, which presumably means reduced psychological resilience coupled with impairment in general health. These deteriorations are provoked by the HPA axis, “which does not function properly in patients with BD”.  Note the term provoked, which isn’t quite the same as caused.  Also note the cautious wording in the final clause:  “does not function properly in patients with BD”.  At first glance, this seems to be saying that the malfunctions cause the “BD”.  But when read more carefully, no such causal connection is stated or even implied.  All that’s being asserted is that HPA malfunction and being labeled BP are correlated.  The causation, if it exists at all, could go either way.
  1. People labeled BP have high cortisol levels as measured by the two tests mentioned.

From all of this, the author concludes:

“From this perspective, HPA axis irregularities seem to be a genetic attribute endowing vulnerability to mood disorders.”

Note the vagueness:  “seems to be” and “vulnerability”.  Not quite the same as cause.

But there’s more.  The evidence for the HPA “irregularities” is the elevated cortisol level, which, incidentally, is just an average figure.  In the study cited, several of the BD “patients” had cortisol levels in the same range as the controls.  But more importantly, it’s been common knowledge since the 50’s that high alcohol consumption is associated with high cortisol levels, and, according to DSM-IV:

“As the Manic Episode develops, there is often a substantial increase in the use of alcohol or stimulants which may exacerbate or prolong the episode.” (p 330)

This is echoed in DSM-5, which notes a

“…tendency for individuals with bipolar 1 disorder to overuse substances during an episode.” (p 131)

So the elevated cortisol may reflect nothing more than frequent heavy drinking.

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

 In general, Dr. Muneer makes no claim that a biological cause to “BD” has been established.  Indeed, the paper is characterized by caution and guardedness in this matter.  For instance:

“…it is probable that most of the cortisol-GR [glucocorticoid receptor]-related mechanisms alluded to above are a sign of the putative genetic underpinning.” [Emphasis added]

Putative means assumed or believed to be the case.

“Given that the mechanisms of HPA axis dysregulation are incompletely known at present, as is its role in dictating the risk of the disease in vulnerable subjects, current work is beginning to unravel the molecular targets of illness development and progression in BD.” [Emphasis added]

“In bipolar patients, major mood episodes of either polarity result in an inflammatory response that has been convincingly shown in several studies.” [Emphasis added]

So the “episodes” cause the biological malfunction rather than the other way round.

Under the heading LIMITATIONS, the author states:

“The following caveats should be kept in mind while deducing any inferences with respect to the neurobiology of BD:
1) Not all predisposed individuals are afflicted by BD, which underscore the issues of genetic epistasis and hitherto little known mechanisms that mediate resiliency.
2) There are large gaps in knowledge due to the absence of good animal models replicating BD.
3) Technological advances are needed to reproduce findings from animal research in human samples.”

Note the truly exquisite optimism in item 1 above.  Not all the people who have the biological correlate in question go on to develop the thoughts, feelings, and actions which psychiatry labels BD.  So these individuals must have some as yet unknown “mechanisms” that confer resilience.  But the alternative perspective, that this is simply not a fruitful line of inquiry, isn’t even addressed.


None of the three studies put forward by Michael as evidence that “mental illness” is biologically caused come even close to establishing this premise.  Indeed, in each case, the authors are quite clear that the evidence for this premise is not to hand.  The articles are essentially discussion papers which discuss the implications of previous research, and express the hope that more definitive findings will be available some time in the future.

Meanwhile, psychiatrists and their supporters continue to claim that “mental illnesses” are real illnesses caused by brain pathology, that need to be corrected by drugs and/or high voltage electric shocks.  These assertions remain unsubstantiated despite decades of highly motivated and lavishly funded research.  For these assertions to acquire even a semblance of validity, psychiatry needs to demonstrate convincingly that all (or at last the great majority) of the individuals “diagnosed” with a particular “mental illness” have a clear and identifiable neural pathology, and that the causation runs from the pathology to the problems of thinking, feeling, and/or behaving in question.  Weak correlations to neurophysiological processes or genetic variations are irrelevant, as I showed in the original article.

And while psychiatrists, for self-serving reasons, continue their inane efforts to “unravel” the neurobiological causes of these so-called illnesses, more obvious natural causes are studiously ignored and neglected.  Tampering irresponsibly with a person’s brain because he is depressed, while ignoring  those features of his lifestyle and recent history that have been known from time immemorial to precipitate depression, is reckless folly.

The Biological Evidence for “Mental Illness”

On January 2, 2017, I published a short post titled Carrie Fisher Dead at Age 60 on Behaviorism and Mental Health.  The article was published simultaneously on Mad in America.

On January 4, a response from Carolina Partners was entered into the comments string on both sites.

Carolina Partners in Mental Healthcare, PLLC, is a large psychiatric group practice based in North Carolina.  According to their website, they comprise 14 psychiatrists, 7 psychologists, 34 Advanced Practice Nurse Practitioners/Physicians Assistants, and 43 Therapists and Counselors.  They have 27 North Carolina locations.

Partners’ comment consists essentially of unsubstantiated assertions, non sequiturs, and appeals to psychiatric authority.  As such, it is fairly typical of the kind of “rebuttals” that psychiatry’s adherents routinely direct towards those of us on this side of the issue.  For this reason, and also because it comes from, and presumably represents the views of, an extremely large psychiatric practice, it warrants a close look.

I will discuss each paragraph in turn.

“We strongly disagree with this article, which neglects a lot of important information and uses selective hearing to distort what Carrie Fisher was about and also to distort the evidence for mental illness as a real disorder.”

My Carrie Fisher article was brief (566 words), and was intended as a counterpoint to the very widespread obituaries that lionized her as a champion of “bipolar disorder”.  The essential point of my article was that Ms. Fisher had been a victim of psychiatry, and like a great many such victims, died prematurely.  Obviously I neglected a lot of important information.  I could have gone into great length as to the recklessness of psychiatry assigning the bipolar label, with all its implications of helplessness, disempowerment, and “chemical imbalance” to a young woman who by her own account was, at the time, using any drugs she could get her hands on.  But I felt that a brief and respectful statement of the facts was all that was needed.

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

“Mental illnesses have a long history of biological evidence. For example, researchers have demonstrated that people with depression have an overactive area of the brain, called Brodmann area 25. Schizophrenia has been linked to specific genes, as PTSD and autism have been linked to specific brain abnormalities. Suicide has been linked to a decreased concentration of serotonin in the brain. OCD has been linked to increased activity in the basal ganglia region of the brain.”

Brodmann area 25 (BA25)
Partners did not provide a specific reference in support of this contention, but my best guess is that the reference is Mayberg, HS, et al (1999) Reciprocal Limbic-Cortical Function and Negative Mood: Converging PET Findings in Depression and Normal Sadness (Am J Psychiatry 1999; 156:675–682).  Here’s the study’s primary conclusion:

“Reciprocal changes involving subgenual cingulate [which includes Brodmann area 25] and right prefrontal cortex occur with both transient and chronic changes in negative mood.”

What this means essentially is that negative mood, whether transient or enduring, is correlated with changes in both the subgenual cingulate (Brodmann area 25) and the right pre-frontal cortex, and that when the depression is relieved, the changes are reversed.

This, of course, is an interesting finding, but provides no evidence that depression, mild or severe, transient or enduring, is caused by a biological pathology.

The reality is that all human activity is triggered by brain activity.  Every thought, every feeling, every action has its origins in the brain.  I cannot lift a finger, blink an eye,  scratch my head, or recall my childhood home without a characteristic brain function initiating and maintaining the action in question.  Without stimuli from the brain, my heart will stop beating, my respiratory apparatus will shut down, and I will die, unless these functions are maintained by machines.

So there is absolutely no surprise in the discovery that sadness and despondency have similar neural triggers and maintainers.  It would be amazing if they didn’t.  But – and this is the critical point – this does not warrant the conclusion that sadness which crosses arbitrary and vaguely-defined thresholds of severity, duration, and frequency is best conceptualized as an illness caused by pathological or excessive activity in BA 25.

Depression is a normal state.  It is the normal human reaction to significant loss and/or living in sub-optimal conditions/circumstances.  It is also an adaptive mechanism, the purpose of which is to encourage us to take action to restore the loss and/or improve the conditions.

All consciously-felt human drives stem from unpleasant feelings.  Thirst drives us to seek water; hunger, food; hypothermia, warmth; hyperthermia, coolness; danger, safety, etc.  Sadness and despondency are no exceptions.  They drive us to seek change, and have been serving the species well since prehistoric times.

But – as is the case with all the above examples – when a drive is not acted upon, for whatever reason, the unpleasant feelings worsen.  Just as unrequited hunger and thirst increase in strength, so the depression drive when not requited deepens.

The reality is that most people deal with depression in appropriate, naturalistic, and time-honored ways.  If the source of the depression is the loss of a job, they start job-hunting.  If the source is an abusive relationship, they seek ways to exit or remediate the situation.  If the source is a shortage of money, they seek ways to budget more sensibly, or increase their earnings; etc.

Depression, either mild or severe, transient or lasting, is not a pathological condition.  It is the natural, appropriate, and adaptive response when a feeling-capable organism confronts an adverse event or circumstance.  And the only sensible and effective way to ameliorate depression is to deal appropriately and constructively with the depressing situation.  Misguided tampering with the person’s feeling apparatus is analogous to deliberately damaging a person’s hearing because he is upset by the noise pollution in his neighborhood, or damaging his eyesight because of complaints about litter in the street.

Our feeling apparatus is as valuable and adaptive as our other senses.  But psychiatry routinely numbs, and in many cases permanently damages, this apparatus to sell drugs and to promote the fiction that they are real doctors.  Their justification for this blatantly destructive activity hinges on the false notion that depression becomes a diagnosable illness when its severity crosses arbitrary and vaguely-defined thresholds.  But deep despondency is no more an illness than mild despondency.  The latter is the appropriate and adaptive response to minor losses and adversity.  The former is the appropriate and natural response to more profound or more enduring adversity.  Though, of course, what constitutes profound adversity will vary enormously from person to person.  An individual, for instance, raised to the expectation of stable and permanent employment may be truly heartbroken at the loss of a job.  Another individual, raised to the notion that there’s always another job “around the corner” will, other things being equal, be less affected.  And so on.

In this regard, it’s noteworthy that Partners’ comment refers to overactivity in BA 25.  The use of the prefix over implies pathology, but in reality there is no yardstick to determine what would be a correct amount of activity for BA 25.  All that can be said, on the basis of Mayberg et al’s findings, and subsequent BA 25 research, is that when a person is sad, there is more activity than when he is happy.  So the use of the term “overactivity” is deceptive – sneaking in the notion of pathology without any genuine or valid reasons to consider it so.  The “reasoning” here is:

–  depression is an illness
–  depression is correlated with high activity in BA 25
–  therefore high activity in BA 25 is pathological

In other words, the contention of pathology rests on the assumption that depression is an illness.  To turn around and use this falsely inferred pathology to prove that depression is an illness is obviously fallacious.  It is also typical of the kind of circular reasoning that permeates psychiatric contentions.  In reality, there is nothing in Mayberg et al or in subsequent research that warrants the conclusion that the increased activity in BA 25 is pathological or excessive.

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

Schizophrenia linked to specific genes
This assertion, that schizophrenia is linked to specific genes, is frequently adduced in these debates, as evidence that “schizophrenia” is a real illness with a biological pathology.  Here again, Partners do not provide any references in support of this assertion, but there have been a number of studies in the past fifteen years or so that have found links of this kind.  However, in all cases, the correlations have been small.  In other words, there are always a great many individuals who have been assigned the “schizophrenia” label, but who do not have the gene variant in question; and there are a great many who have the gene variant, but who do not acquire the label “schizophrenia”.  To date, no genetic test has been found helpful in confirming or refuting a “diagnosis of schizophrenia”.

An additional problem arises here, in that the assertion that “schizophrenia has been linked to specific genes” is often interpreted as meaning that “schizophrenia” is a genetic disease, which it emphatically is not.  To illustrate this, let’s look briefly at a real genetic illness:  polycystic kidney disease (PKD).  This is a well established genetic illness caused by cysts in the kidneys.  The cysts progressively block the flow of blood through the kidneys, causing tissue death.

Most cases of PKD are caused by the defective gene (PKD-1).  In polycystic kidney disease, the pathology occurs because the PKD-1 gene causes the nephrons to be made from cyst wall epithelium rather than nephron 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 is the primary genetic effect.  This structure causes the wall to produce fluid.  As the nephrons become increasingly blocked, the kidneys produce less urine.  So, reduced urination is a secondary effect of the gene PKD-1.  Symptoms of PKD don’t usually emerge until adulthood, but about 25% of children with PKD1 experience pain and other symptoms.  So a child growing up with polycystic kidney disease may feel sick much of the time.  Such a child, other things being equal, is likely to be fussier and more distressed 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.  The fussiness would be a tertiary effect of the gene PKD1.

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.

Cleft palate is another example of a pathology that is caused by a gene defect; actually a gene deletion.  This condition results in a characteristically strained and nasal speech quality which can be quite stigmatizing.  The nasal speech is a secondary effect of the gene 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 speaking as little as possible, by withdrawing socially, or in various other ways.  These reactions would be considered tertiary effects of the defect.  And so on.  As with the PKD, each step in the chain takes us further from the genetic defect, and the statistical associations grow proportionally weaker, and it would be stretching the matter to say that the lack of speech was caused by the gene deletion.  Nor would one conclude that the child’s social withdrawal was a symptom of a genetic disease.  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.  The effects of any minor genetic anomalies that might exist have had ample opportunity to be shaped by social and environmental factors, and these 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 bridge, or read romance novels, visit libraries, play football, or whatever.  If the sample sizes are large enough, and in genetic research sample sizes are often enormous, 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, much less illnesses.

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 piano, for instance, unless one has appropriate neural apparatus, and fingers, both of which require appropriate DNA.  But even a person with good genetic endowment in these regards, will never learn to play unless he is exposed to certain environmental factors.  He must, at the very least, encounter a piano.  In the same way, a person whose genetic endowment might be relatively marginal might become an excellent pianist, if he were to receive persistent 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, and establishing functional habits in interpersonal, occupational, and other important life areas.  Obviously it requires appropriate neural apparatus, hence the weak correlations with genetic material, but equally clearly it calls for a nurturing childhood environment, with opportunities for emotional growth and acquisition of social, occupational, and other skills.

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, and of little or no practical consequence.

Nor is it surprising that the correlations between being labeled “schizophrenic” and various psychosocial factors are by contrast generally strong.  Having a schizophrenia label is correlated with childhood social adversity, childhood abuse and maltreatment, poverty, and a family history of migration.

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

Generally similar considerations apply to Partners contentions with regards to “PTSD”, “autism”, suicide, and “OCD”, but space precludes a detailed discussion here.

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

“Eric Kandel, MD, a Nobel Prize laureate and professor of brain science at Columbia University, says, ‘All mental processes are brain processes, and therefore all disorders of mental functioning are biological diseases…The brain is the organ of the mind. Where else could [mental illness] be if not in the brain?'”

Dr. Kandel (now 87 years old) is an eminent neuroscience researcher at Columbia University.  There’s an extensive biography in Wikipedia.  His early research focused on the neurophysiology of memory.  He has received numerous awards, including the Nobel Prize in Physiology/Medicine (2000), and is widely published.  His record of research achievements is enormous, and his knowledge and expertise are vast, but in the statement quoted by Partners, and, incidentally, by other psychiatry adherents, he is simply wrong.

Let’s take a closer look.  Logically, the Kandel quote can be stated symbolically as:  A is identical to B; therefore malfunctions or aberrations in A are malfunctions or aberrations in B.

On the face of it, this seems sound, and indeed, it is a valid inference in some situations.  For instance, the furnace in a person’s home is the primary heating appliance; therefore, malfunctions in the furnace are malfunctions in the primary heating appliance.  Indeed, in a simple example of this sort, the statement is tautological.  We are simply substituting the synonyms furnace and primary heating appliance, and the inference contains no new information or insights.  But the inference is fallacious in more complex matters.

Let’s concede, for the sake of discussion, that the premise of the Kandel quote is true, i.e., that all mental processes are brain processes.  The term mental processes embraces a wide range of activities, including sensations, perceptions, thoughts, choices, positive feelings, negative feelings, hopes, beliefs, speaking, singing, general behavior, etc.

The term “disorders of mental functioning” is harder to define, but, again for the purposes of discussion, let’s accept the APA’s catalog as definitive in this regard.  Let’s accept that anything listed in the DSM is a “disorder of mental functioning”.

It’s immediately obvious that some of the DSM entries are indeed the result of brain malfunctioning.  In the text these are referred to as disorders due to a general medical condition or to the effects of a substance.  But in the great majority of DSM labels, no such biological cause is identified, and so the conclusion in the Kandel quote would appear to call for some kind of evidence or proof.  However, in the Kandel quote, the conclusion is not presented as something that has been, or even needs to be, proven.  Rather, it is presented as a logical conclusion inherent in, and stemming directly from, the premise.  And it is from this perspective that the Kandel quote needs to be evaluated.

To pursue this, let’s consider the example of “oppositional defiant disorder”.  This is a disorder of mental functioning as defined above, because it is listed in the DSM.  And according to Dr. Kandel’s “logic”, it is also therefore a “biological disease”.  The “symptoms” of oppositional defiant disorder as listed in DSM-5 are:

  1. Often loses temper.
  2. Is often touchy or easily annoyed.
  3. Is often angry and resentful.
  4. Often argues with authority figures or, for children and adolescents, with adults.
  5. Often actively defies or refuses to comply with requests from authority figures or with rules.
  6. Often deliberately annoys others.
  7. Often blames others for his or her mistakes or misbehavior.
  8. Has been spiteful or vindictive at least twice within the past 6 months. (p 462)

Obviously for any of these behaviors to occur, there has to be corresponding neural activity. But there is no necessity that the neural activity is diseased or malfunctioning in any way.  A child learning from his environment, developing his behavioral repertoire in accordance with the ordinary principles or learning, could acquire any or all of these behavioral habits without any malfunctioning in his neural apparatus.  We acquire counterproductive habits as readily, and by essentially the same processes, as we acquire productive ones.  In general, if a child discovers that he can acquire power and control in his environment by throwing temper tantrums, he will, other things being equal, acquire the habit of throwing temper tantrums.  Similarly, if arguing with parents and other authority figures yields positive results, there is a good chance that this also will become habitual.  And this is not because there is anything wrong with the child’s brain.  Rather, it’s because his brain is functioning correctly.  He is internalizing as habits those decisions and actions that pay off.  It is often observed in child-raising practice that if you’re not training your children, they’re training you.

Similar observations can be made about the other seven “symptoms” of oppositional defiant disorder, and indeed all the DSM labels.  A person with a perfectly normal-functioning brain can acquire the habits in question if the circumstances are conducive to this learning.

So to return to the question in the Kandel quote:  “Where else could [mental illness] be if not in the brain?”, the answer is clear:  In the self-serving and unwarranted perception of psychiatrists.  Mental illness is the distorting lens through which psychiatrists view all problems of thinking, feeling, and behaving.  It is the device they use to legitimize their drug-pushing and to maintain the fiction that they are practicing medicine.

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

“You’re right that mental illness is also affected by social and environmental conditions–by a person’s disposition, or upbringing, or current environment. It’s also true that mental illness is affected by drug use (both prescribed and not prescribed). So are other medical conditions, such as heart disease and cancer.”

I’m not sure where Partners are coming from here, because I never made any such statement.  In my view, which I have stated clearly on numerous occasions, “mental illness” is a psychiatric invention, self-servingly created to promote the spurious notion that all problematic thoughts, feelings, and/or behaviors are illnesses.  And not just illnesses in some vague allegorical sense, but real illnesses “just like diabetes”, which need to be treated by medically trained psychiatrists with mood-altering drugs and high voltage electric shocks to the brain.

Partners’ vague concessions concerning environment, child-rearing, and drug effects is a fairly standard psychiatric sop, but doesn’t mitigate their earlier contentions on the “long history of biological evidence” and their uncritical endorsement of the logically spurious Kandel quote.

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

“And it’s true that mental illness is often difficult to diagnose because of
1) the current limitations of the field of research. Thomas R. Insel, MD, director of the National Institute of Mental Health, for example, talks about how the diagnosis and treatment of mental illness today is where cardiology was 100 years ago, concluding that we need to continue scientific research of mental illnesses.  (There’s a longer quote on this below.)”

And (from later in the comment)

“Longer aforementioned quote:
Take cardiology, Insel says. A century ago, doctors had little knowledge of the biological basis of heart disease. They could merely observe a patient’s physical presentation and listen to the patient’s subjective complaints. Today they can measure cholesterol levels, examine the heart’s electrical impulses with EKG, and take detailed CT images of blood vessels and arteries to deliver a precise diagnosis. As a result, Insel says, mortality from heart attacks has dropped dramatically in recent decades. ‘In most areas of medicine, we now have a whole toolkit to help us know what’s going on, from the behavioral level to the molecular level. That has really led to enormous changes in most areas of medicine,’ he says.

Insel believes the diagnosis and treatment of mental illness is today where cardiology was 100 years ago. And like cardiology of yesteryear, the field is poised for dramatic transformation, he says. ‘We are really at the cusp of a revolution in the way we think about the brain and behavior, partly because of technological breakthroughs. We’re finally able to answer some of the fundamental questions.'”

It is at least forty years since I started hearing about psychiatry’s great biological breakthroughs that were just around the proverbial corner, and the promise, if my readers will pardon the pun, is getting a little old.

What’s noteworthy, however, is that in other disciplines, where there is hope or expectation of breakthroughs, the proponents of these endeavors generally wait until the evidence is in, before implementing practices based on these hopes.  In fact, to the best of my knowledge, psychiatry is the only profession whose entire work, indeed, whose entire conceptual framework, is based on “evidence” and “breakthroughs” that are not yet to hand.

Note also the truly exquisite contrast between Partners’ earlier and confident contention that “mental illnesses have a long history of biological evidence” with the assertion here that the “diagnosis” and “treatment” of “mental illness” today is where cardiology was 100 year ago.

Incidentally, Dr. Insel, former Director of the NIMH, also said:

“While DSM has been described as a ‘Bible’ for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been ‘reliability’ – each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment.” (Transforming Diagnosis, 2013)

And let us be quite clear.  “Lack of validity” in this context means that the “diagnoses” don’t actually correspond to any disease entities in the real world.  Note also that Dr. Insel didn’t say poor validity, or low validity.  He said lack of validity – meaning none.

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

Back to the Carolina Partners comment:

“2) mental illness symptoms often overlap with symptoms caused by other illnesses, for example, someone with cancer may also become depressed after diagnosis. Or someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.

While considering all these factors, it is still completely inaccurate to state that there is no biological foundation for mental illnesses. They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones. As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”

This is a little rambling, but let’s see if we can unravel it.

“… someone with cancer may also become depressed after diagnosis.”

This is true.  In fact, I would say that most people who contract serious illness become somewhat sad and despondent.  But this in no way establishes the notion that the sadness should be considered an additional illness.

“…someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.”

This quote contains one of psychiatry’s core fallacies:  that the various “mental illnesses” are the causes of their respective symptoms (as is the case in real illness).  To illustrate the fallacy, consider the hypothetical conversation:

Client’s wife:  Why is my husband so tired all the time?
Psychiatrist:  Because he has an illness called major depressive disorder.
Client’s wife:  How do you know he has this illness?
Psychiatrist:  Because he is tired all the time.

Psychiatry defines major depression (the so-called illness) by the presence of five “symptoms” from a list of nine, one of which is fatigue, and then routinely adduces the “illness” to explain the symptoms.  In reality, the “symptoms” are entailed in the definition of the “illness”, and the explanation is entirely spurious.  There are many valid reasons why a person might feel fatigued, but none of these is because he “has a mental illness”.  Mental illnesses are merely labels with no explanatory significance.  And because of the inherent vagueness in the criteria, they’re not even good labels.

“…it is still completely inaccurate to state that there is no biological foundation for mental illnesses.”

As stressed above, there is a biological foundation to everything we do – every thought, every feeling, every eye blink, every action.  But – and this is the point that seems to evade psychiatry – there is no good reason to believe that the various problems catalogued in the DSM are underlain by pathological biological processes.  And there are lots of very good reasons to believe that they are not.

“They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones.”

I don’t think I’ve ever used the term “make-believe” to describe psychiatric “illnesses”, though I do routinely describe psychiatric labels as invented.  The two terms are not synonymous.  What psychiatry calls mental illnesses are actually nothing more than loose collections of vaguely-defined problems of thinking, feeling, and/or behaving.  In most cases the “diagnosis” is polythetic (five out of nine, four out of six, etc.), so the labels aren’t coherent entities of any sort, let alone illnesses.

But the problems set out in the so-called symptom lists are real problems.  That’s not the issue.  I refer to these labels as inventions, because of psychiatry’s assertion that the loose clusters of problems are real diseases.  In reality, they are not genuine diseases; they are inventions.  They are not discovered in nature, but rather are voted into existence by APA committees.

“As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”

But meanwhile psychiatry has made up its mind.  Within psychiatric dogma, all  significant human problems of thinking, feeling, and behaving are illnesses that need to be “treated” with drugs and electric shocks.

. . . . . . . . . . . . . . . . . 


All of this is interesting, and I suppose it’s important to refute the more or less steady stream of unsubstantiated assertions, fallacious reasoning, and spin that flows from the psychiatric strongholds.

But meanwhile the carnage continues.  There is abundant prima facie evidence that psychiatric drugs are causally implicated in the suicide/murders that have become almost daily occurrences here in the US.  My challenge to organized psychiatry is simple:  call publicly for an independent, definitive study to explore this relationship.  And my challenge to rank and file psychiatrists is equally simple:  pressure the APA to call for such a study.  If what you are doing is unqualifiedly wholesome, safe, and effective, then what do you have to fear?


Allen Frances on the Benefits of “Antipsychotics”

On February 1, Allen Frances, MD, published an interesting article on the Huffington Post blog.  The article is called Do Antipsychotics Help or Harm Psychotic Symptoms?, and is a response to Robert Whitaker’s post of January 27:  “Me, Allen Frances, and Climbing Out of a Pigeonhole.  This post, in turn, was a response to Dr. Frances’s Psychiatric Medicines Are Not All Good or All Bad, which was published in the Huffington Post on January 15.  Readers may remember that I published a critique of this latter article on February 9.

A detailed analysis of the debate between Dr. Frances and Robert Whitaker is beyond the scope of this article.  My primary observation is that in his February 1 response, Dr. Frances does not address the points that Robert made on January 27.  Instead, he sets up caricatures of these points, and dispatches these caricatures with the skill and verve of a shadow-boxer who imagines he is engaged in genuine combat.

My present purpose is to take a closer look at Dr. Frances’s February 1 article, and to spell out some of its implications.  Here are some quotes, interspersed with my comments.

“Bob’s [Robert Whitaker’s] advocacy is ambitious, global, and future oriented- requiring a radical reconception of the US approach to people with psychosis. I am preoccupied more by the desperate, unmet needs of patients living dreadful lives in the current moment. In furthering his long range agenda, I believe Bob is misjudging what is best for severely ill people in the present. His recommended ideal treatment can only have a chance of success in an ideal treatment system. People who might do well with less medicine in his ideal world often get in terrible trouble if they try to stop medicine in our shamefully neglectful real world.”

Note the truly exquisite spin. Robert is “ambitious, global, and future-oriented”, while Dr. Frances is the humble pragmatist rising tirelessly to the daunting challenge of meeting the “unmet needs” of desperate “patients”.

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

“Bob acts as if there is an inherent tension between service users and psychiatric providers. I see the current animosity as an unfortunate and idiosyncratic phenomenon, peculiar to the US, and partly contributed to by Bob’s own passionate and somewhat misleading rhetoric.”

This is a huge issue.  The heart of the matter is that there is “tension” between psychiatrists, on the one hand, and some of their former clients, on the other.  Dr. Frances’s contention is that this conflict is not inherent, but, rather, is “an unfortunate and idiosyncratic phenomenon”, for which Robert Whitaker is, at least partly, to blame.

The reality, of course, is quite different. There is indeed “tension” between psychiatrists and many of their former clients.  This “tension”, which I would call out-and-out conflict, also embraces a very large, and growing, number of other mental health professions and members of the general public.  This conflict has arisen because:

  1. Psychiatry’s definition of a mental disorder/mental illness embraces every significant problem of thinking, feeling, and/or behaving, and psychiatry has been using this definition to medicalize problems that are not medical in nature for more than fifty years.
  1. Psychiatry routinely presents these labels as the causes of the specific problems, when in fact they are merely labels with no explanatory significance.
  1. Psychiatry has routinely deceived, and continues to deceive, their clients, the public, the media, and government agencies, that these vaguely defined problems are in fact illnesses with known neural pathology.
  1. Psychiatry has blatantly promoted drugs as corrective measures for these illnesses, when in fact it is well-known in pharmacological circles that no psychiatric drug corrects any neural pathology. Indeed, the opposite is the case.  All psychiatric drugs exert their effect by distorting or suppressing normal functioning.
  1. Psychiatry has conspired with the pharmaceutical industry in the creation of a large body of questionable, and in some cases fraudulent, research, all designed to “prove” the efficacy and safety of pharma products.
  1. A great many psychiatrists have shamelessly accepted pharma money for very questionable activities. These activities include the widespread presentation of infomercials in the guise of CEUs; the ghost-writing of books and papers which were actually written by pharma employees; the promotion of new drugs and “diagnoses” by paid psychiatric “thought leaders”; the publication of fraudulent advertising in psychiatric peer-reviewed journals; the acceptance of pharmaceutical money by the APA; targeting of captive and otherwise vulnerable audiences in nursing homes, group homes, and foster-care systems for prescription of psychiatric drugs; etc., etc…
  1. Psychiatry’s spurious diagnoses are inherently disempowering. To tell a person, who in fact has no biological pathology, that he has an incurable illness for which he must take psychiatric drugs for life is an intrinsically disempowering act which falsely robs people of hope, and encourages them to settle for a life of drug-induced dependency and mediocrity.
  1. Psychiatry’s “treatments”, whatever tranquilizing effects or transient feelings of well-being they may induce, are almost always destructive and damaging in the long-term, and are frequently administered involuntarily.
  1. Psychiatry’s spurious and self-serving medicalization of every significant problem of thinking, feeling, and/or behaving, effectively undermines human resilience, and fosters a culture of powerlessness, uncertainty, and dependency. Relabeling as illnesses, problems which previous generations accepted as matters to be addressed and worked on, and harnessing billions of pharma dollars to promote this false message is morally repugnant.
  1. Psychiatry neither recognizes nor accepts any limits on its expansionist agenda. In recent years, they have even stooped to giving neuroleptic drugs to young children for temper tantrums, under the pretense that these children have an illness called disruptive mood dysregulation disorder.

The anti-psychiatry movement has been in existence, and vocal, for decades.  But it had been successfully marginalized and ridiculed by pharma-psychiatry until the explosion of Internet access provided a voice that even pharma-psychiatry couldn’t silence.  Robert Whitaker has been a powerful, reasoned, and if I may say, restrained voice in these endeavors, and Mad in America is at this time one of the primary outlets for anti-psychiatry views and information.  But blaming the world-wide anti-psychiatry sentiment on Robert is a bit like blaming news reporters for wars, plagues, famines, and natural disasters.  It’s not only false, but betrays a fundamental disconnect with reality.  The anti-psychiatry movement exists because psychiatry is something fundamentally flawed and rotten.  And it is fundamentally flawed and rotten because its leaders have made it so.

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

“Bob’s misreading fails to take into account the fact that psychotic presentations vary greatly in cause, severity, chronicity, prognosis, and appropriate treatment. Many psychotic episodes are transient. Some are stress related- eg a soldier in combat, a college kid or traveller who becomes delusional when away from home. Some are a transient part of mood disorder and remain quiescent if the mood disorder is successfully treated. Some are related to substance intoxication or withdrawal. Some are caused by head trauma or medical illness. And some normal people have hallucinatory experiences that cause no impairment and have no clinical significance. Transient psychotic symptoms in the above situations may require a short course of antipsychotics, but these should be gradually tapered after the episode has resolved. Generally this can be done without much risk of return of psychosis- assuming the stressor, substance problem, mood disorder, or medical problem has resolved. Bob and I would agree on short term or no antipsychotic treatment for such transient psychoses.”

Once again, note the spin.  Robert Whitaker’s article was about people who had been labeled schizophrenic, but Dr. Frances is “refuting” Robert’s contentions by focusing on “psychotic episodes” that clearly do not meet the APA’s criteria for schizophrenia.  This discrepancy persists throughout Dr. Frances’s post.  In Robert’s article the word “schizophrenia” occurs 12 times, but in Dr. Frances’s response, the word is nowhere to be found.  Dr. Frances is obviously aware of these distinctions, and it’s extremely difficult to put a benign interpretation on this kind of obfuscation.

The central point of Robert’s paper is, I believe, contained in the following passage:

“Every important detail from the conventional narrative, which tells of a great medical advance, can basically be filed under the heading of ‘not really true.’ The arrival of the antipsychotics into asylum medicine did not lead to deinstitutionalization; a change in social policy did. The dopamine theory of schizophrenia arose from an understanding of how drugs acted on the brain, and not from an understanding of what was going on in the brains of people so diagnosed, and when researchers looked to see whether people diagnosed with schizophrenia had overactive dopamine systems as a matter of course, they didn’t find that to be so. The drugs were not like insulin for diabetes. Nor was there evidence that the arrival of the antipsychotics kicked off a great advance in outcomes for schizophrenia patients. Indeed, in a 1994 paper, Harvard researchers reported that long-term outcomes were now no better than they had been in the first third of the 20th century, when water therapies were a mainstay treatment.

In contrast, a scientific understanding of antipsychotics supported the patients’ counter-narrative. Thorazine, Haldol, and other first-generation antipsychotics powerfully blocked dopamine pathways in the brain, which reduced one’s capacity to respond emotionally to the world and to move about it. Hence the zombie feeling. Antipsychotics did cause brain damage, as could be seen in the twitchings of people who developed tardive dyskinesia after years on these drugs. Moreover, research had shown that in compensatory response to the drug’s blockade of dopamine receptors, the brain increased the density of its dopamine receptors, and, there was reason to worry that this increased the person’s biological vulnerability to psychosis. Given these facts, there was plenty of reason for people diagnosed with schizophrenia and other psychotic disorders to want to stop taking them.

In terms of the ‘evidence base’ cited by psychiatry for its use of the drugs, which is held up by psychiatry as its trump card in this battle of narratives, it is easy to see that the evidence for long-term use is flawed. Researchers had conducted any number of studies in which a group of stabilized patients were either maintained on an antipsychotic or abruptly withdrawn from the drug, and with great regularity, the drug-withdrawal group relapsed at a higher rate. This was seen as proving that continual drug use lowered the risk of relapse, and thus provided evidence for maintaining patients indefinitely on the medication. But, of course, another conclusion to be drawn is that the high relapse rate is a drug-withdrawal effect, and not evidence of the long-term risk of relapse in unmedicated patients. The relapse studies also didn’t provide any evidence about how well schizophrenia patients functioned on the drugs, or their quality of life, particularly over the long term.”

Note that the word “schizophrenia” occurs five times in this passage alone, and it is clear that Robert is referring to individuals who have been labeled schizophrenic and who have been “treated” from that perspective.  Dr. Frances’s discussions concerning transient “psychotic episodes” are not pertinent, particularly in the light of psychiatry’s long-held insistence that “schizophrenia” is a life-long degenerative illness.

So it’s not a case of Robert Whitaker misreading the matter, but rather one of Dr. Frances miswriting the matter.

Nor is the miswriting inconsequential.  By juxtaposing the terms “schizophrenia” and “transient psychotic symptoms”, Dr. Frances has managed to convey the impression that he personally favors a more selective and tapered approach to neuroleptic drugs than that which has been typically adopted by psychiatrists since the drugs first came on the market.  This approach has been:  keep taking the “medications” even after a first episode has been successfully “treated”.

Dr. Frances is also conveying the impression that he has favored a less-is-more approached since the ’60s:

“I began my career in psychiatry in the mid 1960s, just when antipsychotics were first being used widely. The new meds dramatically improved psychotic symptoms, but equally dramatically produced dreadful side effects, especially in the ridiculously high doses then being tried.”


“Troubled by this, I was one of the principal investigators on a multisite NIMH funded study testing the feasibility of two new approaches to reducing medication burden. The first was very low dose treatment; the second was expectant treatment, with meds used intermittently only when patients needed them. Patients were randomly assigned to 3 conditions: 1) standard dose injectible med; 2) one-fifth standard dose injectible med; 3) placebo injection with oral meds added as needed. All three groups also received intense individual and family therapy and social support, often done in the home. Many patients in the low dose and expectant groups did well, but the catastrophes were sometimes catastrophic and irreversible. I became convinced that the risks of going off meds for people with chronic psychosis usually overwhelm the benefits. It is the patients’ decision to make, but my advice has been not to rock the boat when chronic psychotic symptoms are responding to meds. Stay on the lowest possible dose, but stay on it over time. When psychosis has been chronic, the risks of discontinuing medication usually far outweigh the benefits.”

As I mentioned in my earlier article, I have been unable to find this particular study, and Dr. Frances provides no reference, so I have no way of ascertaining the methodology or the formal outcome/conclusions.  It does seem odd that Dr. Frances would refer to a piece of research in two successive articles without providing a citation to enable his readers to access the study.

Dr. Frances’s subjective assessment that the “catastrophes were sometimes catastrophic and irreversible” and his equally subjective conviction that “the risks of discontinuing medication usually far outweigh the benefits” are interesting, but obviously are subject to the kind of selection bias that formal studies are designed to overcome.  Dr. Frances saw individuals come off the “meds”, and subsequently crash and burn, but by the same token, those individuals who came off the “meds” and did well, wouldn’t necessarily have come to his attention.  Indeed, it is entirely credible that many of these latter individuals would have actively avoided the ministrations of psychiatry.

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

“Antipsychotics have many grave disadvantages that make them a last resort. They suppress symptoms, rather than curing them. They can cause unpleasant side effects and dangerous medical complications. They contribute to shortened life expectancy. And they are subject to wide overuse even when there is no indication. We should be extremely cautious and selective in their use quite independent of Bob’s tenuous claim that they worsen psychosis.”

This paragraph is interesting, particularly when compared with The Expert Consensus Guidelines for the Treatment of Schizophrenia published by Dr. Frances and his two colleagues, John Docherty, MD, and David Kahn, MD in 1996 (Journal of Clinical Psychiatry, Volume 57, Supplement 12B).  The final chapter in this supplement (p 51-58) is “A Guide for Patients and Families”.  Here are some quotes:

“Schizophrenia is a disorder of the brain like epilepsy or multiple sclerosis.  This brain disorder interferes with the ability to think clearly, know what is real, manage emotions, make decisions, and relate to others” (p 51)

Ongoing antipsychotic medication is necessary in both the acute and preventive phases. During the acute phase, medications help relieve the positive symptoms that are often out of control.  After the acute phase ends, ongoing antipsychotic medication greatly reduces the chances that acute symptoms will recur (a relapse).” (p 52) [Boldface in original text]

“The drugs used to treat schizophrenia are called antipsychotics.  They help relieve the delusions, hallucinations, and thinking problems associated with the disease.  These drugs appear to work by correcting an imbalance in the chemicals that help brain cells communicate with each other.” (p 53)

There is no evidence that the individuals whom psychiatry labels as schizophrenic have an imbalance in their brain chemicals.  Nor is there any evidence that neuroleptic drugs correct any neurological problem.  In fact, they are neurotoxic.

“The newer drugs are called atypical antipsychotics because they are less likely to cause some of the annoying and distressing side effects associated with the conventional antipsychotics.” (p 53)

So, the side effects which today Dr. Frances calls “dreadful”, and which he concedes cause “dangerous medical complications” and “shortened life expectancy”, he characterized in 1996 as “annoying and distressing”.  And this is not because any new information has been uncovered.  The devastating adverse effects of these products had been known for at least 30 years when Drs. Frances, Docherty, and Kahn (incorporated ironically as Expert Knowledge Systems, LLC) produced the document.  And given that the chapter in question is “A Guide for Patients and Families”, it is difficult to interpret this understatement as anything other than a deliberate attempt to deceive the target audience, and to counter any resistance individuals might have to ingesting these products.

“Usually patients respond well to treatment of a first episode of schizophrenia, but if there are repeated episodes or schizophrenia, symptoms sometimes persist despite treatment with the standard antipsychotic medications.  Fortunately, the newer drugs can often help patients whose symptoms no longer respond to the standard antipsychotic medications.  For such patients, the experts recommended that risperidone be tried first.” (p 53)

Incidentally, the Treatment Guidelines were funded by a grant from Janssen Pharmaceutica, the manufacturer of risperidone.  The promotion of risperidone, which is clearly evident throughout the guidelines, is not a coincidence.  It has been reported (here) that on July 3, 1996, Drs. Frances, Docherty, and Kahn (as Expert Knowledge Systems) wrote to Janssen:

“We are also committed to helping Janssen succeed in its effort to increase its market share and visibility in the payor, provider, and consumer communities.” (p 16)

This matter is in the public record (Texas v. Janssen LP, D-1GV-04-001288, District Court, Travis County, Texas), and has been reported by several writers, including Paula Caplan, PhD, but has never, to the best of my knowledge been addressed by Dr. Frances or either of his colleagues, although the venality of the statement is extreme even by psychiatric standards.  Drs. Frances, Docherty, and Kahn were reportedly paid $515,000 by Johnson and Johnson (owners of Janssen) for their work on the guidelines.

Back to the Treatment Guidelines document:

“The good news is that schizophrenia is very treatable.  A cure for schizophrenia, like diabetes, has not yet been found, but the symptoms can be controlled with medication in most people.  Prospects for the future are constantly brighter through the pioneering explorations in brain research and the development of many new drugs.  To achieve good results, however, you must stick to your treatment and avoid substance abuse.  Be sure to take your medicine as directed.  Even if you have felt better for a long time, you can still have a relapse if you stop taking your medication.” (p 54) [Boldface in original text]

“Because people with schizophrenia have to take their medications for a very long time, often for their whole life, it is very important to recognize and try to treat any side effects they may have from these medications.” (p 54)

“For patients who don’t take their medication regularly, more active interventions are likely to be needed to be sure the patient takes medications.  There are community treatment programs in which staff frequently go see patients and may give them their medications.  For such patients, the experts also recommended day hospitals where patients go 3-5 days a week and participate in several hours of programming that help insure that medication is taken.” (p 56) [Italics in original text]

“The most important factor in keeping patients with schizophrenia out of the hospital is having them take their medications regularly.  The best compliance with treatment is obtained when the family works with the patient to help him or her remember the medicine.  Sometimes long-acting injectable forms of medication are used when patients find it hard to take a pill every day.” (p 57)

The above quotes call into question Dr. Frances’s present assertion that coming off the “meds” is “the patient’s decision to make”.  This is even clearer in the guidelines proper where under the heading “Intervention During Continuation and Maintenance Treatment”, it states unambiguously:

Medication responsive patient – frequently not compliant   ■ Assertive community treatment (ACT);  Day hospital with medication management. (p 11)

There are a great many other passages in the schizophrenia treatment guidelines that indicate that Drs. Frances, Docherty, and Kahn promoted the use of neuroleptic drugs on a more or less indefinite basis.  The Schizophrenia Treatment Algorithm on pages 13 and 14, for instance, sets out in schematic form the treatments and adjustments that should be made in a variety of emerging situations.  In none of these situations is it suggested that the “medications” be stopped or that such a move even be considered.

But, in fairness to Dr. Frances and his colleagues, I have to acknowledge that there is a section headed “Psychosocial interventions” on page 11 of the guidelines.  Here’s the entire passage:

Psychosocial intervention

  • Ensure continuity from inpatient to outpatient care (e.g., schedule first outpatient appointment within 1 week of discharge, give enough medication to last until that appointment, telephone follow-up if patient misses appointment)
  • Psychoeducation for family to support and encourage medication compliance”

Incidentally, in the treatment algorithm mentioned earlier, under the neuroleptic complication “Agitation or insomnia”, only one intervention is given:  “Add benzodiazepine”.

In this context it needs to be stressed that the Schizophrenia Treatment Guidelines were widely distributed and influential.  Indeed, this was the intention from the start.  Here’s another quote from David Rothman’s expert testimony:

“The guideline team [Drs. Frances, Docherty, and Kahn] promised wide distribution of its product, including publication in a journal supplement.  The team was prepared to have J&J participate in its work, not keeping the company even at arms length.  With a disregard for conflict of interest and scientific integrity, the group shared its drafts with J&J.  On June 21, 1996, Frances wrote Lloyd [John Lloyd, J&J’s Director of Reimbursement Services]:  ‘We are moving into the back stretch and thought you would be interested in seeing the latest draft  of the guidelines project….Please make comments and suggestions.’  (Italics added).  So too, the group was eager to cooperate with J&J in marketing activities.  Frances wrote without embarrassment or equivocation:  ‘We also need to get more specific on the size and composition of the target audience and how to integrate the publication and conferences with other marketing efforts’  (Italics added)” (p 15)

Back to Dr. Frances’s current article:

“This debate does have serious real world consequences.  There is no more momentous decision in the life of someone who has had psychotic symptoms than whether or not to stop meds- and it always comes up in the treatment, often repeatedly. If the person’s symptoms have been brief and not life threatening, I fully encourage a decision to gradually taper and then stop. It is, under these circumstances, definitely worth the fairly minor risk of relapse to avoid the major risk of medication side effects and complications. Many of Bob’s most enthusiastic followers are in this category- harmed by prolonged overtreatment for transient problems.”

But there’s a catch 22.  For a “diagnosis of schizophrenia”, the DSM requires the presence of two or more of five “characteristic symptoms” for a significant portion of time during a one-month period “or less if successfully treated” [emphasis added].  And when this “diagnostic” determinant is coupled with psychiatry’s long-standing preference to use the drugs as the “treatment” of first resort, it is clear that the concept of transience in this context becomes meaningless.  There is no way of knowing if a person’s “symptoms” have been brief, if they are routinely suppressed with neuroleptic drugs as soon as they become evident.  The individual is still eligible for a “diagnosis of schizophrenia”, (a “life-long disease”) and will be pressured relentlessly by psychiatrists and the mental health system to continue to take the “meds” indefinitely.  And this is a situation to whose making Dr. Frances has been a major contributor.

Of course, we can all make mistakes, and we can all learn from our mistakes.  And if Dr. Frances is saying that his earlier enthusiasm for neuroleptic drugs and his downplaying of the entailed risks were mistakes, that would be one thing.  But to suggest that he has always been a proponent of moderation and restraint in this area is, I suggest, a distortion of the readily checkable historical facts.

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

Interesting as all these matters are, there is a much more fundamental issue that seldom gets aired:  the nature and effects of neuroleptic drugs.  In recent years, psychiatrists and pharma have been promoting the term “antipsychotics” for these products, denoting that they eliminate, or correct, psychotic thoughts in the same way, for instance, that antibiotics eliminate germs.  In fact, the term antipsychotic is much more a marketing device than an accurate descriptor, and it is to psychiatry’s shame that they have adopted and promoted the term so enthusiastically.  What these drugs are, and what they were originally called, is major tranquilizers.  Back in the 60’s and 70’s, their action was routinely likened to piling damp grass on a fire.  The fire wouldn’t go out, but its action and intensity were greatly reduced.  Nor are the actions of these products specific to psychotic thoughts and speech.  They suppress all activity.  In fact, they don’t normally eliminate delusions or hallucinations; rather they render the individual indifferent to them.  In the 50’s, the action of chlorpromazine, the first major tranquilizer, was likened to a chemical lobotomy.

A second factor that needs to be recognized is that people very seldom enter psychiatry’s orbit on the grounds of craziness alone.  One can be as crazy as one likes in the privacy of one’s home.  And indeed, I suggest that most of us adhere to some notions that would meet psychiatry’s definition of delusions:  “A false belief based on incorrect inference about external reality that is firmly held despite what almost everyone else believes and despite what constitutes incontrovertible and obvious proof or evidence to the contrary.” (DSM-5, p 819).  I, for instance, believe that there are no mental illnesses:  that the medicalization of all significant problems of thinking, feeling, and/or behaving is a hoax, designed to enhance psychiatry’s prestige, and to sell pharma products.  I occasionally receive emails and comments suggesting that I must be crazy to entertain such ideas, and I suppose, from psychiatry’s point of view, my beliefs could be considered delusional. But, oddly enough, I’ve never been picked up on a 72-hour hold, or court-ordered to have a psychiatric evaluation.  Even if I were to stand peacefully on the sidewalk in front of a mental health center distributing anti-psychiatry pamphlets, it is unlikely that I would be molested, though I might be asked to keep a certain distance back from the door and not to impede pedestrian traffic, etc…

But, if I go inside the building and start noisily and agitatedly berating the psychiatrists, and tearing down the pharma-distributed infomercial posters, I will likely be arrested within five minutes.  And if I continue to express my views in a loud and agitated manner at the police station, and if my general presentation seems odd or eccentric, it is possible that I will be remanded to a psychiatric facility for a 72-hour evaluation, and will be assigned “a diagnosis of schizophrenia”.

This is the critical point.  It is the expression of unusual or non-conformist views, coupled with expressions of anger, agitation, and aggression, that precipitates many of these “diagnoses of schizophrenia” and subsequent “medical” incarcerations.  It is certainly possible for an individual to find himself in this situation without any display of anger or agitation.  But in many cases, it is presentations of this kind that draw official attention and result in civil commitment, incarceration, and forced drugging, even though the person may not have committed any crime.  And yet, amazingly, it is almost unheard of for these interventions to entail any inquiry into the source(s) of the agitation or any attempt to ameliorate the anger in any way other than with tranquilizing drugs.

The central issue is not whether “antipsychotics” are effective in the treatment of “schizophrenia”, but rather, whether major tranquilizers are effective in the suppression of anger, agitation, and aggression.  And of course, they are, provided we discount the fairly common adverse effect of akathisia, the manifestation of which, incidentally, according to Dr. Frances’s own Guidelines, may be confused with – and the irony of this is beyond words – “psychotic symptoms”. (p 55).  (In other words, one of the long-established adverse effects of the drugs is to make a person seem crazy – and, presumably, eligible for more “treatment”!)  But, for the most part, the drugs are strong tranquilizers which reduce general activity and speech, and dampen feelings and emotions.

Neuroleptic drugs have often been called chemical straightjackets.  And the question as to whether or not these products should be used to control agitation, anger, and aggression, is not a medical matter.  It is a human rights/legislative issue.  The use of physical restraints by law enforcement officers is subject to ongoing legislative and judicial oversight, but the use of chemical restraints by psychiatrists is effectively unregulated.  The fundamental question is not:  are antipsychotic medications effective in the treatment of schizophrenia, but rather:  is it morally acceptable to use major tranquilizers, that have devastating adverse effects, as chemical restraints, frequently for years and even decades?  It is time to start calling a spade a spade; and it is beyond time for legislative and judicial bodies to recognize the abuse and deception in this area and to take appropriate action.  There is a pressing need to recognize that these products are not medications in any ordinary sense of the term.  They are chemical restraints.

Are ‘Psychiatric Disorders’ Brain Diseases?

Steven Reidbord MD is a board-certified psychiatrist who practices in San Francisco.  He writes a blog called Reidbord’s Reflections.  On December 12, 2015, he posted an article titled Are psychiatric disorders brain diseases?  It’s an interesting and thought-provoking piece, with many twists and turns.

Here are some quotes, interspersed with my comments and reflections.

“Of the conditions deemed inherently psychiatric, some seem rooted in biological brain dysfunction.  Schizophrenia, autism, bipolar disorder, and severe forms of obsessive compulsive disorder and melancholic depression are often cited.  It’s important to note that their apparently biological nature derives from natural history and clinical presentation, not from diagnostic tests, and not because we know their root causes.  Schizophrenia, for example, runs in families, usually appears at a characteristic age, severely affects a diverse array of mental functions, looks very similar across cultures, and brings with it reliable if non-specific neuroanatomical changes.  Even though schizophrenia cannot be diagnosed under the microscope or on brain imaging, it is plausible that a biological mechanism eventually will be found.  (The same type of reasoning applied to AIDS before the discovery of HIV, and to many other medical diseases.)  A similar argument can be made for other putatively biological psychiatric disorders.”

This is a complex paragraph.  Dr. Reidbord names five psychiatric “diagnoses” and expresses the belief that they seem “rooted in biological brain dysfunction”.  He stresses that their apparently biological nature derives from their appearance (natural history and clinical presentation), and not from diagnostic tests or a knowledge of any pathology involved.

As an example of this, he states that “schizophrenia”

  • runs in families
  • usually appears at a characteristic age
  • severely affects a diverse array of mental functions
  • looks very similar across cultures, and
  • is associated with reliable, though non-specific, neuroanatomical changes

And, it has to be acknowledged, that, at first look, these five factors, if present, might constitute grounds to suspect brain dysfunction. But let’s take a closer look.


A “diagnosis of schizophrenia” is based on the presence of two or more of the following:

  1. delusions
  2. hallucinations
  3. disorganized speech
  4. disorganized behavior
  5. apathy or avolition

It seems obvious to me that each of these behaviors (or lack of behaviors, in number 5) can be passed on from generation to generation through normal social learning, without any assumption of a genetically-mediated pathology.  If I, for instance, believe that airplane contrails contain toxic substances that are being spread by the government as part of a sinister plan to render the citizens docile and debilitated, and if I had communicated these concerns to my children during their formative years, there is a good chance that one or more of them would have accepted these assertions at face value, and might even pass them along to their children in turn.

Similarly if my growing children had witnessed me responding to stimuli that were clearly internal rather than external, or speaking in a markedly disorganized way, there would be, I think a reasonable expectation that one or more of them might also acquire these habits through social learning.

And so on for the other three “symptoms”.  There is no need to assume genetic transmission in these behaviors.  Indeed, an assumption of genetic transmission of any behavior is always doubtful.  Genes transmit biological structure.  Structure has an impact on behavior, obviously, but there are always multiple intervening factors.


I have addressed this issue at some length in earlier posts (here, here, and here).  But for the present purposes, it is perhaps sufficient to note that the “characteristic age” for the “onset of schizophrenia” is during the transition from late adolescence to adulthood (i.e. about 17 to 25).  For a majority of the population, this is probably the most difficult period of life, especially because it comes at a time when we are particularly inexperienced in dealing with complex challenges.   It is a period during which many people experience a good deal of failure, disappointment, embarrassment, and discouragement.  All of which can push an individual towards a negative perspective, and in severe cases to a state of belief that would qualify as “delusional”, without any assumption of a “biological brain dysfunction”.


These are not so diverse really.  The APA criteria essentially identify:  false/mistaken beliefs; responding to internal stimuli; lack of organization in speech and behavior; and apathy/joylessness.  But only two of these need to be present in any given individual.


This issue has become almost impossible to address in any methodical way, because western influences (including the influence of the DSM) have reached virtually every corner of the globe.  The DSM has become the distorting lens through which all problematic behavior is viewed and assessed, and there are enormous formal and informal incentives for psychiatrists everywhere to find “diagnoses”.

But in 1963, these influences were considerably weaker and less widespread.  In that year, Henry Murphy, MD, et al sent questionnaires about “schizophrenia symptoms” to psychiatric centers in various parts of the world, and received responses from 27 countries.  Here’s how they summarized their results:

“The main significance of our findings at this stage is that doubt has been thrown on the picture which Euro-American psychiatry has built up of the schizophrenic process.  For instance, considering the high percentages of the simplex and catatonic sub-types of schizophrenia reported for certain Asian samples (in some instances our respondents kindly sent actual figures) and the low percentages of the paranoid sub-type, it might be questioned whether the delusional systems which are the most familiar feature of chronic schizophrenia in Euro-American hospitals are an essential part of the disease process.  Might they not be culturally conditioned attempts by the personality to ‘make sense’ of that process, attempts which Eastern cultures inspire to a much lesser degree?” (pp. 248-249 Murphy HBM et al, A cross-cultural survey of schizophrenic symptomatology, International Journal of Social Psychiatry, 1963, 9: 237-249)

Dr. Murphy et al are obviously committed to the disease concept, but their finding of such cultural diversity casts doubt on the universality of “schizophrenia”.

And in 1973, E. Fuller Torrey, MD, prior to his conversion to biological reductionism, reviewed the evidence on the universality of schizophrenia, and summarized the matter:

“In fact, however, there is no evidence upon which to base a belief in the universality of schizophrenia.  The studies which have been used to support this belief are found, on careful examination, not necessarily to point in this direction at all.  If anything, they may lead to the opposite conclusions:  Schizophrenia may not be a universal disorder.” (p. 53 Is schizophrenia universal? An open question, Schizophrenia Bulletin, 1973, 7: 53-59)


“‘Once an idea becomes part of a textbook, it develops a life of its own and is seldom questioned.  This is what has occurred with the idea that schizophrenia is universal.'” (ibid, p 56)


“Finally, within the past few years some preliminary data on schizophrenia in New Guinea have become available. Burton-Bradley, a psychiatrist who has been there for a decade and a half, reported 343 cases of schizophrenia among the first 1,000 cases of mental disease which he examined. Virtually every one of the cases, however, occurred among individuals who had been living in the larger towns (‘the person of limited cultural contact, the so-called bush individual, very rarely presents with the symptoms of schizophrenia [Burton-Bradley 1969]’) or who had just migrated from rural areas to the towns (‘Not uncommon is the acute schizophrenia of sudden onset coming on usually within three months of  the patient’s leaving the village and working for the first time in a large town. Such patients readily recover and are returned to their village, at which level they can function without disturbance [Burton-Bradley 1963]’)” (ibid p 57.  The Burton-Bradley reference is:  Burton-Bradley, B.G. Culture and mental disorder.  Medical Journal of Australia, 15:539-540, 1963)

So, the fact that “schizophrenia” looks similar across cultures is more likely to reflect an artifact of cultural colonialism than any intrinsic property of the so-called illness.  And this is not merely a matter of psychiatrists seeing what they expect to see.  Once the “diagnosis” has been made, psychiatrists and other mental health workers actually begin a process that consists essentially of training the individual in how to “be schizophrenic”.  This process entails “educating” the client on the “symptoms and course of the illness”, and encouraging him to self-identify with the label.


Dr. Reidbord doesn’t specify which changes he has in mind.  The main change of this nature that comes to my mind is brain shrinkage, but I think that there is broad consensus at present that this is more a function of extended use of neuroleptic drugs than any putative underlying disease process.

. . . . . . . . . . . . . . . . 


The analogy to AIDS prior to the discovery of HIV is unconvincing.  All the “symptoms” of the various psychiatric disorders that Dr. Reidbord mentions are behaviors, feelings, or thoughts.  And for each, there are plausible and eminently credible explanations from psychology, sociology, and indeed from ordinary experience and common sense.  But the symptoms of AIDS are clearly indicative of biological dysfunction. These symptoms include:

  • Fever
  • Chills
  • Rash
  • Night sweats
  • Muscle aches
  • Sore throat
  • Fatigue
  • Swollen lymph nodes
  • Mouth ulcers

It would be quite a stretch to conceptualize this cluster of symptoms as anything other than a biological malfunction.  But it is entirely plausible to think of “schizophrenia” in this way.  And indeed, Dr. Reidbord himself is restrained in his conclusion:

“Even though schizophrenia cannot be diagnosed under the microscope or on brain imaging, it is plausible that a biological mechanism eventually will be found.  ” [Emphasis added]

In my view, it is considerably more plausible that such a biological mechanism will not be found. This is particularly the case in that more than a hundred years of highly-motivated and generously funded searching for this “holy grail” of psychiatry has to date found nothing.

. . . . . . . . . . . . . . . . 

But all of this, important as it is, is not the main point of Dr. Reidbord’s paper.  Let’s go on.

“Lately, however, some big names in psychiatry have taken a more ideological stance, declaring that psychiatric disorders in general are brain diseases — right now, no further proof needed.  Dr. Charles Nemeroff, widely published professor and chairman of psychiatry at the University of Miami Miller School of Medicine, writes:

In the past two decades, we have learned much about the causes of depression. We now know from brain imaging studies that depression, like Parkinson’s disease and stroke, is a brain disease.

Dr. Thomas Insel, recent director of the National Institute of Mental Health (NIMH) wrote:

Mental disorders are biological disorders involving brain circuits…

Psychiatrist and Nobel laureate Dr. Eric Kandel says:

All mental processes are brain processes, and therefore all disorders of mental functioning are biological diseases.

These claims by prominent psychiatrists agitate critics.  No biomarker for any psychiatric disorder has yet been identified. Genetic vulnerabilities have been discovered, but nothing resembling a smoking gun.  Functional brain imaging reveals biological correlates of mental impairment, not etiology, and no such imaging can diagnose a specific psychiatric condition.  Our best account for most mental disorders remains a complex interaction of innate vulnerability and environmental stress, the ‘diathesis-stress model’.  These psychiatric leaders know the research as well as anyone. How can they call psychiatric disorders brain diseases without scientific proof?”

At this point, readers might be thinking that, despite his earlier comments on biological brain dysfunction, Dr. Reidbord is arguing on our side of the debate.  But wait!  The argument progresses.

“The brain mediates all mental activity, normal or not.  Consequently, any psychiatric intervention — or influential life experience — acts upon the brain.  This is not a new discovery.”

 “It is a philosophical position, monism as opposed to Cartesian dualism, not a scientific finding.”

 “Psychiatric ‘brain disease’ is neither an exaggeration nor a lie.  It does not require scientific proof — and brain imaging has neither strengthened nor weakened the case.  For as long as one is not a philosophical dualist, it is surely true.  In theory, all psychology can be reduced to electrochemical events in brain cells. All psychopathology can be reduced to aberrant electrochemical events, i.e., brain disease.”

Dr. Reidbord is entirely correct in stating that the brain mediates all mental activity.  It also mediates all physical activity.  I cannot lift a finger, shed a tear, recall my mother’s face, hum a tune, feel sad, or even absent-mindedly scratch my ear, without the corresponding neural activity occurring within my brain, and eliciting the thought, feeling, or action in question.

Dr. Reidbord is also correct in stating that, in theory, all psychology can be reduced to electrochemical events within and between brain cells.  In theory, a super-neurologist could identify exactly what happens in a child’s brain when the child learns that two plus two is four; or what happens in a person’s brain when he/she becomes depressed or happy or plays the piano, etc… But the key phrase here is: “in theory”.  This is because, firstly, the complexity and miniaturization of the brain’s circuitry probably precludes the possibility that this kind of detailed super-analysis will ever be feasible. Secondly, and more importantly, a detailed micro-analysis of an event can never capture the kind of qualitative factors that emerge from a macro-analysis.

Take, for instance, the action of a five-year-old boy kicking his teacher in the shin.  Let us pose the question:  Why did he do that?

Our super-neurologist – in theory – could give us a complete account of the entire neurochemical sequence, from the activation of the first sensory neuron to the activation of the last muscle fiber.  In theory, this account, which would run to millions (perhaps billions) of words, would, if accurate, constitute a complete and accurate answer to the question posed above.

A psychological assessment of the incident, however, might conclude that the boy had been raised in a violent home, had never been trained in effective anger control, routinely reacted violently when confronted or given instructions, and that the teacher had told him to stop running around the classroom and to sit down. So he had kicked her.

A sociological perspective might note that the frequency of such attacks in classrooms was increasing generally, and might note associations between this kind of violence and parental conflict, unemployment, cultural background, etc.

The critical point here is that although each account is describing the same incident, there are qualitative differences between them that are critically important.  The neurological account, no matter how complete and thorough it is, could never capture the uniquely human dimensions of the interaction, any more than the psychological account could capture the extraordinary complexity of human biology.  The issue here is not which account is correct, but rather which account is more suited for a given purpose.  If the purpose is to understand human biology, then the neurological account is more helpful.  But if the purpose is to understand the child’s actions and develop corrective measures, then the psychological account is clearly the preferred approach.

And this, of course, takes us straight to the heart of the psychiatric hoax:  that all significant problems of thinking, feeling, and/or behaving constitute brain diseases and are best ameliorated by modulating neurological activity.

Which in turn takes us to Dr. Reidbord’s conclusion in the above quote:

“All psychopathology can be reduced to aberrant electrochemical events, i.e., brain disease.”

And unlike his earlier premises, this conclusion is false.

The best way to illustrate this fallacy is with some examples, but first let’s clarify the language.  “Psychopathology” is a complex term, subject to diverse interpretation.  So rather than try to define this term, let’s use the APA’s Diagnostic and Statistical Manual as a starting point, and accept, for discussion’s sake, that any “diagnosis” or “symptom” listed in the manual constitutes “psychopathology”.

Childhood temper tantrums, for instance, are listed in the DSM as “symptoms” of oppositional defiant disorder, disruptive mood dysregulation disorder, and intermittent explosive disorder.  Therefore, according to Dr. Reidbord, temper tantrums of the severity and frequency specified for these “diagnoses”, “can be reduced” to aberrant electrochemical events.  The phrase “can be reduced to” in this context clearly means “can be conceptualized as”, or “are caused by”.  And the phrase:  “Aberrant electrochemical events, i.e. brain disease”, clearly means:  a malfunction in neurological equipment.

But in fact, a child can acquire the habit of throwing temper tantrums without any neurological malfunction.  Generally speaking, there are two principal ways in which a child can acquire this, and other, habits: learning from results; and learning from imitation/coaching.


If a child throws a temper tantrum, and the tantrum produces a positive result (e.g. a parent yielding to his demands), then, other things being equal, there is an increased probability that temper tantrums will become habitual, especially if they continue to produce the same kind of outcome.  This is not a function of aberrant electrochemical events in the brain cells.  In fact, it is exactly the opposite:  a perfect example of the normal human learning apparatus operating flawlessly.  It is not an example of something going wrong in the brain, rather it is an example of something going right.  We humans learn from the results of our actions, an obvious fact that has been verified experimentally countless times, and in addition accords perfectly with common sense and general observation.  And we acquire functional, productive habits in exactly the same way and by means of the same cognitive apparatus as counter-productive and problematic habits.  Acquiring the temper tantrum habit is particularly easy, in that babies are born with an anger apparatus which needs little encouragement to express itself in rage and aggression.  In fact, the opposite is the case:  teaching anger control is the challenge.


Imitation is another major component of our normal learning apparatus.  The child acquires skills and habits through imitating, at first his parents and siblings, and later individuals outside the home.

It is self-evident that through imitation and coaching a child can acquire habits that are useful and helpful; but it is equally obvious that he can also acquire habits that are destructive and counter-productive.  Through imitation a child can, for instance, learn to fear objects that are dangerous, but through precisely the same mechanism, he can learn to fear harmless objects such as spiders, closed-in spaces, open spaces, cats, hypodermic needles, air travel, dogs, heights, elevators, social gatherings, etc… All of these fears are “psychopathological” in the sense specified above, but all can be acquired, through imitation, by a person with a perfectly normal-functioning brain, provided the fear in question is being modeled by a significant person in the child’s life.  It is fallacious to assume brain pathology based solely on the fact that the acquired behaviors/feelings are counter-productive or distressful.

Similar observations can be made with regards to every “symptom” listed in the DSM.  Habits of paranoid speech, incessant speech, over-eating, self-deprecating speech, grandiose speech, rule-breaking, cruelty, violence, stealing, suicidal threats, suicidal gestures, apathy, etc., can all be acquired by a person with a normally-functioning learning apparatus, either through learning from results or learning by imitation, or both.  In the absence of specifically identified and credibly causative brain pathology, this is the most reasonable and parsimonious way to conceptualize the acquisition of these kinds of habits.

In his ground-breaking monograph, “The Jack-Roller” (1930), Clifford Shaw provides graphic, first person accounts of how a child can acquire the habit of stealing in this way.  For example:

“On the trips with William, I found him to be a rather chummy companion.  I regarded him, not as a brother, but rather as a boy friend from another home.  He was five years my senior.  He sort of showed it in his obvious superiority.  But I didn’t seem to notice that fault.  He was a ‘mamma’s boy’ at home, but oh, Lord, how he changed on our trips!  He taught me how to be mischievous; how to cheat the rag peddler when he weighed up our rags.  He would distract the peddler’s attention while I would steal a bag of rags off the wagon.  We would sell the rags back to the victimized peddler.  He also took me to the five and ten cent store on Forty-seventh Street, and would direct me to steal from the counter while he waited at the door.  I usually was successful, as I was little and inconspicuous.  How I loved to do these things!  They thrilled me.  I learned to smile and to laugh again.  It was an honor, I thought, to do such things with William. Was he not the leader and I his brother?  Did I not look up to him?  I was ready to do anything William said, not because of fear, but because he was my companion.  We were always together, and between us sprang up a natural understanding, so to speak.

One day my stepmother told William to take me to the railroad yard to break into box-cars.  William always led the way and made the plans.  He would open the cars, and I would crawl in and hand out the merchandise.  In the cars were foodstuffs, exactly the things my stepmother wanted.  We filled our cart, which we had made for this purpose, and proceeded toward home.  After we arrived home with our ill-gotten goods, my stepmother would meet us and pat me on the back and say that I was a good boy and that I would be rewarded”

And stealing is psychopathology:  a “symptom” of “conduct disorder”, “kleptomania”, and “antisocial personality disorder”, but I suggest it is clear that there is nothing wrong with the narrator’s neuro-cognitive apparatus.  He isn’t learning the behaviors approved by the dominant culture.  But he is learning the rules of the smaller group to which he belongs and feels connected.

The habits of thinking, feeling, and behaving mentioned above make perfect sense when viewed from the individual’s perspective, but appear counter-productive and dysfunctional from the perspective of so-called “normality”.  But within the context of psychiatry’s intractable commitment to the medical model, the search for a “diagnosis” precludes any search for meaning or sense in the “patient’s symptoms”.  For psychiatry, the “patient” is “sick”.  His brain is assumed, without evidence, to be broken.  There is no meaning or sense to his “symptoms”.  And in this way, psychiatry has locked itself in a cocoon of comforting but destructive and condescending certainty, which they show no inclination to leave.

. . . . . . . . . . . . . . . . 

At this point, Dr. Reidbord’s paper takes another interesting twist:

“Without elucidating the causative mechanisms, however, this reductionism amounts to little more than political rhetoric.  Calling psychiatric disorders brain diseases serves no clinical or research purpose, it only serves political ends: bringing psychiatry into the fold as a ‘real’ medical specialty, impressing Congress and other funding sources, perhaps allaying stigma.  As a tactic it smacks of insecurity and self-aggrandizement, wholly unbefitting a serious medical specialty.”

To which I would certainly agree, adding only that the reductionism also constitutes an invalid inference, as outlined above.

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

“Freud’s psychoanalysis acts on brain cells, and ultimately alters chemical bonds in those brain cells.  We could rename psychoanalysis and psychotherapy ‘verbal neuromodulation.’  But to what end?  A reductionistic account of this sort, festooned with pseudoscientific verbiage, has no practical significance.

Brain research is a young field.  It should be vigorously pursued for what will surely be learned.  If history is any guide, many conditions currently considered psychiatric will eventually be explained biologically — and ironically, they will no longer be psychiatric conditions, as was the case with Huntington’s disease, brain tumors, lead poisoning, and many other diseases that now belong to other medical specialties.

Stumping for psychiatry as clinical neurobiology will be justified when basic research in this area affects clinical practice. Until then, ‘brain disease’ is only a philosophical technicality, a spin, to give our clinical work and the institution of psychiatry an air of scientific credibility.  Particularly in light of how diseases leave psychiatry once they are well understood, the field should embrace uncertainty, not preempt it with the premature use of brain disease language.”

So what we’ve got here is an interesting and curious mix of very commendable honesty and professional self-interest coupled with the oft-heard psychiatric assertion that sometime in the future the brain pathologies will be discovered.  In the meantime, Dr. Reidbord contends that promoting clinical neurobiology is not justified, and will not be justified until basic research affects clinical practice.

But, in my view, Dr. Reidbord misses the essential point:  that the “real-illness-just-like-diabetes” assertion has been, and continues to be, widely and avidly promoted by psychiatry, and that clinical practice is already based almost entirely on the false contention that all problems of thinking, feeling, and/or behaving are best conceptualized as neurological illnesses.  It is extremely rare to encounter, or even hear about, a psychiatrist who offers any kind of “treatment” other than drugs or high voltage electric shocks to the brain.  On his website, Dr. Reidbord tells us that his clinical practice “skews towards dynamic psychotherapy” and that he has “a healthy skepticism of commercial influences on medical practice.”  Again, this is commendable but rare.

Dr. Reidbord downplays the practical significance of the “aberrant electrochemical events” falsehood by calling it a philosophical position rather than a scientific finding.  But from either perspective, it is problematic.  From the former it is fallacious (as shown earlier); from the latter it is non-existent (such research does not exist).  Nevertheless, it is widely promoted within psychiatric circles, and is routinely used to medicalize non-medical problems, and to legitimize the use of dangerous drugs to “treat” an ever-increasing range of human problems.

. . . . . . . . . . . . . . . . 

And, incidentally, in another interesting twist in the paper, Dr. Reidbord actually seems to be saying something very similar to this:

“Freud could then have made it a point to declare, as Drs. Insel and Kandel do now, that all mental disorders are biological diseases.  No additional science was required even a century ago.

He didn’t because there was nothing to gain.  The best treatments at the time were psychological, not biological.  There was no grant money at stake, no research agenda to support.  The status and livelihood of early psychoanalysts did not depend on their treatment being biological.”

In other words, if I’m understanding Dr. Reidbord correctly, psychiatry is positing the brain disease concept today because it is good for business.  And in this, of course, he is absolutely correct.  But, ironically, by asserting the falsehood that “all psychopathology can be reduced to aberrant electrochemical events, i.e. brain disease” Dr. Reidbord is himself contributing to, and legitimizing, the hoax.




DSM-5 defines delusions as “…fixed beliefs that are not amenable to change in the light of conflicting evidence.”  (p 87).  The manual lists six kinds of delusions:  persecutory; referential; grandiose; erotomanic; nihilistic; and somatic.  The APA provides another definition of delusions on p 819.  It’s substantially the same as the one above, but offers the additional varieties:  bizarre; delusional jealousy; mixed type; mood-congruent; mood-incongruent; of being controlled; thought broadcasting; and thought insertion.  Interestingly, nihilistic delusions are omitted from the second list.  These, we are told on page 87,  “…involve the conviction that a major catastrophe will occur.”

A person who groundlessly believes that his neighbors are plotting to kill him, for instance, is considered to be manifesting a persecutory delusion.  A person who groundlessly believes that he/she is the object of another person’s love and devotion, is considered to be manifesting an erotomanic delusion. And so on.  It is clear that the APA’s definition of a delusion is not specific enough for consistent application.  For instance, 26% of American adults believe that the Sun goes around the Earth every day, despite abundant, and readily available, information to the contrary. But this is not a psychiatric delusion, even though it clearly meets the requirements of the definition.

In general, beliefs that are  “…ordinarily accepted by other members of the person’s culture or subculture…” are specifically excluded from the APA’s definition (p 819).  The ramifications of this exclusion are particularly interesting.  Suppose, for example, that I develop the patently false notion that I am a descendant of the great French Emperor Napoleon Bonaparte, and that as such, I am the rightful emperor of Europe, psychiatry would describe me as delusional, and if my speech were a little incoherent, and my manner aloof (as befitting an emperor!), I might easily attract a “diagnosis of schizophrenia”, especially if I started making a nuisance of myself.

Now schizophrenia, as any psychiatrist can tell you, is a brain illness.  The brain is broken, and this causes the symptoms.  So my grandiose delusions are caused by brain pathology.  But now let’s thicken the plot, so to speak, and imagine that I begin to attract enormous numbers of adherents to my cause.  The disenchanted masses of the Old World rush to my standard, overthrow their venal and rapacious leaders, and propel me to my rightful and long-deserved status.  Now, my belief, because of the culture/subculture exclusion, is no longer a delusion.  So the brain pathology, that had previously afflicted me so grievously, is cured by popular acclaim!  This is a strange illness!

Obviously this last example is a little tongue-in-cheek.  But the underlying reality is entirely valid:  a patently false, even bizarre, belief is a product of brain damage.  But it is not a product of brain damage if enough people believe it.  The APA doesn’t specify how many believers are required to effect this miraculous cure, but the use of the term “sub-culture” suggests that it doesn’t have to be all that many.

Up till about 1960, many, perhaps most, psychiatrists believed that unusual beliefs of this kind had some meaning or significance within the context of the person’s history and needs.  A person who had been particularly disempowered, for instance, might express the delusion that he was the Emperor of Russia.  Or a person who needed to be cared for might express somatic delusions.  And so on.  Psychiatric treatment often consisted of talking to the person to explore these kinds of interpretations, and to look for alternative perspectives.  But this kind of approach is now almost entirely defunct within psychiatric circles.  Today, false beliefs of the kind mentioned above are almost invariably seen as symptoms of a brain disease, to be eradicated by neurotoxic chemicals and/or electric shocks.  In passing, it is worth noting that psychiatrists believe that these drugs and shocks constitute medical treatment of an illness – a belief that is generally not amenable to change, despite abundant contrary evidence.  But that’s a long tangent.

Brains, of course, can and do malfunction, and it is certainly conceivable that on some rare occasions, false beliefs might be a function of brain damage.  But in the vast majority of psychiatric clients who have been “diagnosed” with a delusional disorder, there is no established history of brain pathology.  So the question arises, why do people with perfectly ordinary and well-functioning brains  sometimes cling to false beliefs despite abundant contrary evidence?


Relative to our size, we human beings have big brains, and they enable us to do some extraordinary things.  For instance, they enable us to remember things.  The electronic storage of data is a commonplace matter today, and many people imagine that the human brain functions something like a hard drive.  In fact, the brain is infinitely more subtle.  The computer stores whatever you put into it.  The brain does not.  The human brain is not an elaborate tape recorder.  At any given instant, our brains are presented with literally millions of individual stimuli to choose from.  From its earliest moment, the brain learns to select.  This is critical, because selection inevitably involves distortion.

We learn to select on the basis of our needs.  Our cognitive apparatus, like the rest of our physical equipment, is in the service of our needs.  As children, we learned to pay attention to the things we needed to pay attention to.  We learned which parts of our world were important in terms of getting our needs fulfilled.  Children learn very quickly what they have to do in order to get fed, or cuddled, or approved of, or read to, or whatever.  But – and this is a critical point – what works for one child in one family doesn’t work for another.  Most children seek the approval of their parents. A child growing up in a rabidly racist home learns to say the n….. word.  He also learns to think the n….. word.  He learns to focus on pieces of information which portray black people in a bad light, and to screen out information complimentary to black people.  Children raised in blue collar families are often taught to distrust establishment figures.  Children raised in wealthy homes learn to distrust labor associations.  And so on.

We all were taught how to think, by our parents, educators, and circumstances.  Some people learned to think in a very open, accepting way.  Others learned to be narrow and suspicious.  Some people were taught that wisdom lies in dogmatic pronouncements; others were taught that wisdom requires questioning and exploration.  Some learned that the world is a beautiful place.  Others learned that it is a vale of tears.  Some learned that it is an opportunity for rapacious exploitation.  Others learned that it is a minefield to be traversed with infinite caution.

Thought styles change over time.  People who grew up during the depression learned to value money and thrift.  This is because they frequently went hungry.  If you had a dime you could get a loaf of bread.  If you didn’t have a dime, you didn’t eat.  People raised in the fifties enjoyed greater affluence, and frequently are exasperated by what they perceive as the neurotic penny-pinching concerns of their parents.  The important point is that both groups are right.  Both groups learned to think in a manner appropriate to the environment in which they were raised.


A child who is beaten savagely day after day comes to think of the world as a hostile place.  He screens out the positive attributes of parental figures, and of authority figures generally, and focuses on their potential to hurt.  He conceptualizes the adult world as an obstacle course.  His basic need is to navigate as painless a path as possible.  On the other hand, the child on whom every attention is lavished conceptualizes the adult world as if it were a huge cherry orchard.  His primary need is identifying the biggest cherries, and getting an adult figure to hoist him up to pick them, or, better still, pick them for him.  Both children are conceptualizing the world correctly.

The human cognitive apparatus is not a disembodied logic machine.  It is an integral part of the person, and is in the service of his or her needs.  This is not to say that we are permanently enslaved by the attitudes of our childhood.  People obviously can and do develop their own thought patterns.  But equally, it is probably overly optimistic to imagine that we can ever completely transcend the basic concepts and mindsets that we developed early in life.

Most of the “delusional thinking” that is diagnosed in mental health practice is in fact nothing more than the perfectly normal outcome of a painful (or otherwise extreme) childhood.  But in order to recognize this, one has to spend a great deal of time listening to the individual, validating his concerns, empathizing honestly and sincerely – and most of all – recognizing that he/she is fundamentally understandable: a human being with all the potential, positive and negative, that this implies.  Psychiatry, however, with its 15-minute med-checks, and its catalog of spurious illnesses, sees the “delusional thinking” as a neuro-pathological condition.  Consequently, no attempt is made to explore these kinds of origins.  In fact, the content of the unusual thinking is almost always completely ignored.


Another key concept in understanding “delusional thinking” is the notion of failure.  At the risk of stating the obvious, we all fail at something from time to time.  Some of our failures are minor – like spilling a glass of water.  Others are major – like  crashing the car, or getting fired from a job.  When confronted with a failure, however, we always have two conceptual options.  We can acknowledge that we messed up, and take corrective action; or we can distort our perception of the situation to such an extent that it no longer seems to be a failure.

For example, if I try to install a pane of glass in a window frame, and in the process the pane breaks, I have two broad options.  I can identify what I did wrong, and resolve to be more careful with the replacement.  Or I can scream and yell at my wife for distracting me at a critical point in the operation.  Or I can assert that the glass had a flaw in it; the glass cutter was dull, etc..  I can, if I work at it a little, persuade myself that the breakage was not really my fault.

Similarly, if I am fired for incompetence in my job, I can conceptualize this as a failure on my part, and take some appropriate action.  Or I can conceptualize it in a way which exonerates me from blame.  (The vice-president wanted my job for his son-in-law, etc…)

The issue here is not which explanation is the true one.  Truth isn’t always that cut and dried.  The issue is that there are always multiple ways to conceptualize our errors.  Most of us don’t experience an inordinate amount of failure, but when we do, we can always resort to the second option to salve our wounded egos.  Our friends and loved ones intuitively recognize the process, and no great harm is done.

When a person experiences massive amounts of serious failure, however, the situation is very different.  In such cases, the need to distort reality becomes progressively stronger with each new incident, and eventually the person can reach a state where his thought patterns are quite bizarre.  What needs to be recognized is that these thought patterns provide him with the comfort that he cannot achieve through normal successful interaction with his environment.

The reasons for this kind of persistent failure are highly individualized, but generally involve unrealistic expectations, coupled with inadequate training and preparation.  In many cases, there is also a history of abuse.  Transition from adolescence into adulthood is one of the most difficult things any of us ever have to do. Unfortunately, at that age, most of us were reluctant to admit that we were experiencing any difficulty, or to ask for help.  The three major tasks at that period are:  selecting and launching a career, partner selection, and emancipation from parents.  Many people fail disastrously in one or more of these areas.  Some pick themselves up and try again (Option One).  Others withdraw from the field, and subconsciously rationalize this withdrawal by developing an increasingly negative view of the mainstream world.

There is really nothing startling or new in this way of conceptualizing thought distortion.  Most people can recognize this, and can even recount incidents when they themselves responded to a failure in this way.  What is startling, however, is that modern psychiatry never attempts to explore this aspect of distorted thinking.  According to psychiatry, the client thinks in this odd, bizarre fashion because he/she has a brain disease.  Nothing more needs to be explored.  All he/she needs to do is eat some major tranquilizers every day and return to the clinic once a month to be checked for adverse effects.  And psychiatry clings to this notion despite the fact that decades of generously funded and highly motivated research have failed to identify the brain pathology in question.


Another explanation for odd beliefs is that they may be true.  At one period in my life I lived in central Appalachia.  One of our neighbors was an elderly farmer.  We shared about a quarter mile of fence at the ridge-line, and often found ourselves working together setting posts and stringing wire.  During these encounters, he would explain to me the difficulties involved in farming in such hilly country.  But the special bane of his existence was a noxious weed called Multiflora Rose.  This is a rather delightful-looking green bush which develops a profusion of soft white flowers in springtime.  Unfortunately – for the farmers – it spreads like fury, and is virtually indestructible.  It is not unusual in parts of Appalachia to see whole pastures taken over by this resilient intruder.  The elderly farmer informed me with a great deal of bitterness that the government was responsible for this plague.  “They brought it here and planted it in our fence lines,” he explained.  At the time, this seemed a little implausible to me, but I later found out that Multiflora Rose was in fact introduced by state governments in Appalachia during World War II.  At that time, steel for barbed wire was scarce, and the agricultural experts hit on the idea of using the resilient plant as a living fence.  Programs were established, and farmers were encouraged financially to plant the rose in their fence lines.  Unfortunately, the experts had grossly underestimated the plant’s ability to spread, and today there are government-funded programs to eradicate the troublesome rose.

What’s interesting about this matter is that had the farmer expressed his belief, that the bushes had been planted by the government, in a mental health clinic, this might well have been considered delusional, and might even have attracted a “diagnosis of schizophrenia”.  Mental health practitioners almost never try to check the truth of bizarre stories they hear from their clients.  And once a psychiatrist hears what appears to be a bizarre or odd belief, his radar goes to full sensitivity, and, primed by the DSM’s simplistic formulas, he begins to “see” other symptoms of the “diagnosis” in question.

In addition, it should be recognized that the validity or otherwise of an unusual belief is not just a matter of factual accuracy.  In my experience, people who express delusions of grandeur are often individuals who have been massively disempowered, first by their families, schools, and peer groups, and subsequently by psychiatry.  Their insistence that they have special powers can, I think, be accurately interpreted as a functional, though awkwardly voiced, refusal to accept this disempowerment.  Similarly, people who express persecutory delusions often have a long history of being victimized, though not necessarily in the ways that they assert.

These individuals may be factually incorrect in many of their specific assertions, but they are not wrong in their general experience and contentions, that the “normal” world can be extremely dehumanizing, exploitative, indifferent, and intolerant.  Very often their delusions, though incoherent and false to the casual listener, constitute a formidable indictment of a society that not only throws away things, but also throws away people.  And they are often people who have experienced the callousness and disregard of others at first hand.


The essential point here is that the thinking which mental health practitioners call delusional is simply an extreme case of a completely normal phenomenon – namely, the ability of human beings to construct thought patterns which serve our needs, and to consistently screen out information which threatens these patterns.

The psychiatric explanation is invalid, but it is also extremely destructive.  Consider the case of a young man who experiences a series of disastrous experiences throughout late adolescence and early adulthood:  acne; ridicule from peers; ethnic discrimination; social gaffes; obesity; not being “cool”; chronic embarrassment; no sexual contacts; academic inadequacies; inability to find a job on leaving school, etc…  Option One (facing the difficulties and doing something about them) becomes extremely difficult – perhaps even impossible.  The tendency to distort reality – to construct a delusional world of his own – is strong.  And that’s what many such young people do.  The delusional system is simply his way of protecting himself from the reality.  His delusional system is not essentially different from the individual cognitive constructs that the rest of us use.  His is only more highly developed.  And it is more highly developed because he had a greater need to screen out the conventional world.  We are all driven inexorably to find joy.  And if we can’t find it in mainstream thoughts and activities, we look for it somewhere else.

If our deluded young man becomes sufficiently disturbing to his family or friends, or to the community at large, he may attract the attention of mental health practitioners.  He will be questioned by psychologists, psychiatrists, and social workers, all of whom subscribe to the psychiatric dogma, and he will probably be diagnosed as “schizophrenic”.  The destructive aspect of this process is that he now has an “incurable illness” that purports to explain, not only his present situation, but also his previous experiences, and encourages him to give up any attempt to find a fulfilling and satisfying life-role.  So he can remain an outcast for the rest of his life.  The real problems, his series of painful experiences, failures, emotional distress, and lack of coping skills, are ignored.  No attempt is made to teach him the skills that he lacks, or even allow him to vent about his previous misfortune.  Within the mental health system, he will be given neuroleptic drugs, and assigned a “sick” role.  He will be diligently trained in this role, and will be punished in various ways if he deviates from this role.  The chances that a practitioner will ever set foot inside his home are extremely slim.  No attempt will be made to help him achieve functional independence and fulfillment.  In fact, the accepted wisdom in psychiatric circles is that “schizophrenics” should not be pushed, and expectations should be kept to an absolute minimum.  Not surprisingly, the results are pretty dismal.

Allen Frances ‘Replies’


On June 19, 2015, I published a post titled Allen Frances’ Ties to Johnson & Johnson.  In that post, I set out some very serious allegations against Dr. Frances.  I drew these allegations from a document titled Special Witness Report dated October 15, 2010.  The report was written by David Rothman, PhD, Professor of Social Medicine at Columbia College of Physicians and Surgeons.

Dr. Rothman’s report was produced in the context of a lawsuit filed by the State of Texas against Janssen Pharmaceutica, a subsidiary of Johnson & Johnson.

The allegations against Dr. Frances and two other psychiatrists, John Docherty, MD, and David Kahn, MD, arise from their production of an expert consensus schizophrenia treatment guidelines document.  The essential allegation is that Dr. Frances and his two partners violated, to a marked extent, the ordinary standards regarding conflicts of interest in the preparation and publicizing of the guidelines.

I quoted some passages from Dr. Rothman’s article, perhaps the most telling of which is the following:

“EKS [i.e., Drs. Frances, Docherty, and Kahn] wrote to Janssen on July 3, 1996 that it was pleased to respond to its request to ‘develop an information solution that will facilitate the implementation of expert guidelines.’…It assured the company:  ‘We are also committed to helping Janssen succeed in its effort to increase its market share and visibility in the payor, provider, and consumer communities.’”  [Emphasis added]

Paula Caplan, PhD, a clinical and research psychologist, and an Associate at Harvard’s DuBois Institute, had written an earlier article on this topic in Aporia.  Dr. Caplan had titled her article Diagnosisgate: Conflict of Interest at the Top of the Psychiatric Apparatus, and on March 6, 2015, Dr. Frances had published a very weak and ineffective rebuttal titled ‘Diagnosisgate’ Deconstructed and Debunked

. . . . . . . . . . . . . . . . 

Last Sunday, June 21, 2015, Dr. Frances tweeted to  me:  “Setting the record straight on careless claims” with a link to his earlier rebuttal.

So, to set the record straight:

Dr. Frances’s rebuttal did not address a single issue from the David Rothman report, and his tweeted claim that the rebuttal set the record straight is nothing short of fanciful. 

In my article, I challenged Dr. Frances to respond to two questions:

  1. Are the allegations against him and his EKS partners that are set out in detail in the David Rothman report accurate?
  1. Are the quotations in that report that are attributed to Dr. Frances accurate?

This challenge still stands.

The allegations against Dr. Frances are extremely serious, and in my view, comparable misconduct in reputable professions would result in censure, or even expulsion.  But with very few exceptions, the silence from psychiatry on this issue has been deafening, even though the David Rothman report has been in the public arena for almost five years.

At the present time Dr. Frances is presenting himself as the champion of moderation, and he routinely lays the blame for the overuse of psychiatric drugs on pharma marketing and on general practitioners.  But he has never, to the best of my knowledge, acknowledged that in the preparation and dissemination of the Tri-University Guidelines, he and his partners formed what they described as a “strategic partnership” with Janssen, and expressed a firm commitment to “helping Janssen succeed in its effort to increase its market share…”  And to guard against any misunderstandings, the issue here is not that Dr. Frances helped Janssen increase its market share.  The issue is that he did this in the guise of producing an objective treatment guidelines document.

Why aren’t psychiatrists screaming in protest?  Where is the outrage and censure?  Is psychiatry truly so intellectually and morally bankrupt that they will turn a blind eye to virtually anything, provided it expands psychiatric turf?

Allen Frances’ Ties to Johnson & Johnson


I recently came across an article titled Diagnosisgate: Conflict of Interest at the Top of the Psychiatric Apparatus, by Paula Caplan, PhD.  The article was published in Aporia, the University of Ottawa nursing journal, in January 2015.  Aporia is “a peer-reviewed, bilingual, and open access journal dedicated to scholarly debates in nursing and the health sciences.”

Dr, Caplan is a clinical and research psychologist, and an Associate at Harvard’s DuBois Institute.  She worked as a consultant to the DSM-IV task force in the 1980’s, but resigned from this position after two years.    Here’s a quote from her February 2014 post on Mad in America The Great “Crazy” Cover-up: Harm Results from Rewriting the History of DSM:

“In the late 1980s, I was a consultant to two committees appointed by DSM-IV Task Force head Allen Frances to decide what DSM-IV should contain. I resigned from those committees after two years because I was appalled by the way I saw that good scientific research was often being ignored, distorted, or lied about and the way that junk science was being used as though it were of high quality . . . if that suited the aims of those in charge. I also resigned because I was increasingly learning that giving someone a psychiatric label was extremely unlikely to reduce their suffering but carried serious risks of harm, and when I had reported these concerns and examples of harm to those at the top, they had ignored or even publicly misrepresented the facts.”

Dr. Caplan has also written a brief synopsis of the Diagnosisgate article here.


The central theme of Dr. Caplan’s 2015 article is that in 1995, Allen Frances, MD,  and two other psychiatrists (John Docherty and David Kahn) received grants of about $515,000 from Johnson & Johnson to write “Schizophrenia Practice Guidelines” which specifically promoted Risperdal (a Johnson & Johnson product) as the first line of treatment for schizophrenia.  The guidelines were called the “Tri-University Guidelines” in recognition of the fact that Dr. Frances worked at Duke, Dr. Docherty at Cornell; and Dr. Kahn at Columbia.  Subsequently, the three psychiatrists formed Expert Knowledge Systems, and from that platform, actively assisted Johnson & Johnson in the implementation and marketing of the guidelines.  For these latter services, J & J paid EKS a further $427,659.

The role of the three psychiatrists came to light because in 2004, the State of Texas filed a lawsuit against Janssen Pharmaceutica, a subsidiary of Johnson & Johnson, alleging that  company officials “targeted Texas Medicaid with their sophisticated and fraudulent marketing scheme” (here) to ensure that Risperdal was included in the state’s preferred drug list.

During these proceedings, an expert witness report was presented to the court by David Rothman, PhD, professor of Social Medicine at Columbia University College of Physicians and Surgeons.  The report is titled simply “Expert Witness Report” and is dated October 15, 2010.  The report, which can be found here, runs to 86 pages, and is meticulously detailed.

Here are some quotes from Dr. Caplan’s article:

“Allen Frances, arguably the world’s most powerful psychiatrist, spearheaded a massive, million-dollar project using psychiatric diagnosis to propel sales of a potent and dangerous drug by pharmaceutical giant Johnson & Johnson (J & J). Frances began the initiative in 1995, but his involvement has been little known, despite a court document written in 2010 that revealed what its author [David Rothman, PhD], an ethics specialist, called serious deception and corruption in that project.”

“According to the court document, Frances led the J & J enterprise that involved distortion of scientific evidence, conflicts of interest, and other illegal and unethical practices.”

“Rothman reported that, in 1995, the very year after DSM-IV appeared, Johnson & Johnson had paid more than half a million dollars (USD) to Frances and two of his psychiatrist colleagues to create an official-seeming document as the basis for promotion of one of their drugs. The following year, the drug company paid them almost another half million dollars to continue and expand the marketing campaign.”

“According to the Rothman report, Frances and his colleagues wrote guidelines that were designed specifically to persuade physicians to prescribe J & J’s drug Risperdal as the first line of treatment for schizophrenia.”

Here are some quotes from David Rothman’s report:

“In 1993, GTFH Public Relations echoed what State and Federal Associates [another PR company] had recommended the year before.  It, too, emphasized the need [for J & J]to cultivate state officials along with members of the psychiatric community…GTFH also emphasized that J&J should be convening Expert Task Force Meetings: ‘Formulate position and draft guidelines for consensus…Use: ‘Personalized invitational campaign to maximize participation.’…Finally, it counseled J&J to ‘Form exclusive partnership with growing advocacy group,’ citing NAMI as one case in point. J&J should help establish chapters and co-sponsor educational programs on patient issues…”(pp 13-14) [Emphasis added]

Note that one of GTFH’s recommendations was to “…draft guidelines…”

“As one of its first activities, and in disregard of professional medical ethics and principles of conflict of interest, in 1995 J&J funded a project led by three psychiatrists at three medical centers (Duke, Cornell, and Columbia) to formulate Schizophrenia Practice Guidelines.  From the start, the project subverted scientific integrity, appearing to be a purely scientific venture when it was at its core, a marketing venture for Risperdal.  In fact, the guidelines produced by this project would become the basis for the TMAP [Texas Medication Algorithm Project] algorithms, giving a market edge to the J&J products in Texas.” (p 14)

The production of the practice guidelines involved polling a selected sample of expert psychiatrists, and collating their questionnaire responses.

“The guideline team [Drs. Frances, Docherty, and Kahn] promised wide distribution of its product, including publication in a journal supplement.  The team was prepared to have J&J participate in its work, not keeping the company even at arms length.  With a disregard for conflict of interest and scientific integrity, the group shared its drafts with J&J.  On June 21, 1996, Frances wrote Lloyd [John Lloyd, J&J’s Director of Reimbursement Services]:  ‘We are moving into the back stretch and thought you would be interested in seeing the latest draft  of the guidelines project….Please make comments and suggestions.‘  (Italics added).  So too, the group was eager to cooperate with J&J in marketing activities.  Frances wrote without embarrassment or equivocation:  ‘We also need to get more specific on the size and composition of the target audience and how to integrate the publication and conferences with other marketing efforts”  (Italics added)…Indeed, from the start J&J had made it apparent to the team that this was a marketing venture.  In a letter to Frances, Lloyd set forth what he called an ‘aggressive time line’ for the project, and added:  ‘There are a number of other Treatment and Practice Guidelines for schizophrenia being developed or published during this same period that may well serve our marketing and implementation needs at a substantial lesser cost.’…” (p 15)

“Not only were Frances, Docherty and Kahn ready to violate standards of conflicts of interest in mixing guideline preparation with marketing for J&J, but also in publicizing the guidelines in coordination with J&J.  The three men established Expert Knowledge Systems (EKS).  The purpose of this organization was to use J&J money to market the guidelines and bring financial benefits to Frances, Docherty, and Kahn.” (p 15)

“EKS [i.e., Drs. Frances, Docherty, and Kahn] wrote to Janssen on July 3, 1996 that it was pleased to respond to its request to ‘develop an information solution that will facilitate the implementation of expert guidelines.’…It assured the company:  ‘We are also committed to helping Janssen succeed in its effort to increase its market share and visibility in the payor, provider, and consumer communities.’  Now that the ‘first phase’ was completed, with the guidelines created, ‘EKS is now ready to move forward in a strategic partnership with Janssen.’…The strategy will allow Janssen to ‘Influence state governments and providers….  Build brand loyalty and commitment with large groups of key providers around the country.’…EKS also promised ‘rapid implementations,’ with particular attention to having an impact on Texas decision making.’It is our intent to work with the State of Texas immediately in implementing this product in a select number of CMHC’s with the assistance of A. John Rush, MD.’…Again EKS emphasized:  ‘It is essential for Janssen to distinguish Risperidone [Risperdal] from other competitors in a timely and creditable way.’…In its Summary of the document, EKS wrote: ‘Your investment in the development of state of the art practice guidelines for schizophrenia is already beginning to pay off in terms of positive exposure in the Texas Implementation project.’…” (p 15-16) [Emphasis added]

Back to Paula Caplan’s article:

“On August 30, 2012, Texas Attorney General Abbott issued a press release to announce that Texas and 36 other states had together reached a settlement in which Janssen was to pay the states a total of $181 million because of its ‘unlawful and deceptive marketing.’  Here there appears another mystery: Interestingly, nowhere in either the filing or the press release did the names of Frances, Docherty, or Kahn appear, although their deceptive guidelines were the foundation for the enterprise, nor did they include the names of the other psychiatrists whom Janssen had hired to carry out the deceptive acts. Furthermore, they did not include information about harm done to the individuals who had been prescribed Risperdal.”

“Papers impelled by J & J were published in scholarly journals and, as Rothman reports, ghost-written by individuals selected by J & J, with high-profile names affixed as first authors after the articles had been written. These papers helped promote use of Risperdal to treat not only Schizophrenia but also Childhood Onset Schizophrenia, Schizo-affective Disorder, Bipolar Disorder in Children and Adults, Mania, Autism, Pervasive Developmental Disorder other than Autism, Conduct Disorder, Oppositional Defiant Disorder, Psychosis, Aggression Agitation, Dementia, below average IQ, and disruptive behavior. Subsequent to the production and marketing of the Tri-University Guidelines came the FDA approval of Risperdal to treat adults and then children diagnosed with Bipolar Disorder, and finally children diagnosed with Autism.”

And another quote from David Rothman:

“J&J turned the guidelines into a powerful marketing tool.  The slides presented at a CNS National Sales Meeting in March 1997, instructed employees to use the guidelines to convince its ‘Primary customers: P & T members [Pharmacy and Therapeutics committees], Formulary Decision Makers and Psychopharmacologists’ – those who made purchasing and reimbursement decisions – that they should use the guidelines to justify making Risperdal the drug of choice.…J&J also wanted the guidelines to promote the product’s use among ‘Secondary Customers,’ namely ‘Physicians who are not convinced of RISPERDAL’s 1st line status.’  So although the front piece for the guidelines described them as ‘suggestions for clinical practice,’ from J&J’s perspective, they provide ‘credibility; Reinforces RISPERDAL’s 1st line status; Differentiates RISPERDAL from convention[al] APS [antipsychotics] and other atypical APS.’  To make certain the customers got the message, the ‘Full Supplement [of the guidelines publication] should be left behind.’  J&J also funded CME offerings to publicize the guidelines, including a ‘Free ½ Day Seminars, Earn Up to 8 Hours of CE/CME.’  The panel of experts included Frances, Docherty, and Kahn, and also John Rush (who would play a key role in TMAP).  http://web.archive.org/web/19961106071503/www.ibh.com/expert1.htm” (p 17)

. . . . . . . . . . . . . . . . 

What’s particularly noteworthy in all of this is that since about 2010, Dr. Frances has been critiquing the obviously expansionist agenda of DSM-5, and the corruptive role of pharma in disease-mongering, and in the increasing over-use of psychiatric drugs.

In this context, he presents himself as the defender of moderation and scientific integrity, but, to the best of my knowledge, he has never publicly acknowledged his marketing role  with J & J in the creation of the Tri-University Guidelines.


On March 5, 2015, Dr. Frances did respond to Paula Caplan’s “Diagnosisgate” article.  Here are some quotes from this response, which appeared on the Huffington Post blog.  The quotes are interspersed with my comments.

“…in her usual dramatic and distorted way, Dr. Caplan feels she can score points and gain public attention by exposing a supposed, creatively named, ‘Diagnosisgate.'”

It is my general perception that when people respond to criticism with this kind of personal attack, they have something to hide.

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

“Dr. Caplan, as always, is careless with facts, quick with misinterpretations, and filled with wild accusations. I will first debunk what is simple nonsense in her claims and then discuss the issues that do have a factual basis.”

“It is nonsense to state that my participation in guideline development was in any way a conflict of interest with DSM IV or affected in any way its preparation. The guideline project occurred several years after DSM IV was already in print. The term ‘Diagnosisgate’ is no more than Dr Caplan’s misleading attempt to attract an audience and has no connection to reality.”

There is no suggestion in Dr. Caplan’s article that Dr. Frances’s participation in the guideline development was a conflict of interest with DSM-IV.  In fact, Dr. Caplan notes that J & J’s first payment to Drs. Frances, Docherty, and Kahn occurred the year after DSM-IV was published.  What’s stressed in both Paula Caplan’s and David Rothman’s reports is the fact that Dr. Frances and his two co-founders of EKS actively collaborated with Johnson & Johnson in the marketing of Risperdal, and that the guidelines that they created were clearly designed for this purpose.

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

“It is nonsense to imply that I made a great deal of money from DSM IV sales, which Dr. Caplan states totalled $100 million.”

There is no reference, or even implication, in Dr. Caplan’s article, that Dr. Frances made a great deal of money from DSM-IV sales.  Dr. Caplan mentions the fact that sales of the manual “earned more then $100 million”, but there is no suggestion that Dr. Frances shared in these profits.  Again, what’s stressed in both Paula Caplan’s and David Rothman’s articles is that Dr. Frances and his colleagues made about $900,000 from J & J for producing and marketing the Tri-University Guidelines.

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

“It is nonsense for Dr. Caplan to claim there was ‘data distortion’ in either DSM IV or in the guidelines. Both efforts were the result of completely transparent and forthright processes. Both efforts had very clear and published methodological rules of the road that were conscientiously followed every step of the way.”

The phrase “data distortion” occurs in a sub-heading in Dr. Caplan’s synopsis article, but the phrase does not occur in her main article in Aporia.  So I’m not sure exactly what she had in mind.  But the notion that following one’s own “clear and published methodological rules of the road” guarantees validity and lack of bias is a little naïve.  All that Drs. Frances, Docherty, and Kahn would have to do to skew the results is, firstly, select questionnaire recipients whom they knew favored risperidone, and secondly, word the questions in a way that would tend to elicit the kind of responses that would promote risperidone.  In the published guideline document, the authors state that questionnaire participants were selected from several sources:

“…recent research publications and funded grants, the DSM-IV advisers for psychotic disorders, the Task Force for the American Psychiatric Association’s Practice Guideline for the Treatment of Patients with Schizophrenia, and those who have worked on other schizophrenia guidelines.” (p 2)

From this – obviously very large group – Dr. Frances and his partners selected 99 psychiatrists, 87 of whom responded to the questionnaire.  I can find no information as to how the 99 psychiatrists were selected.

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

“She enjoys being the center of controversy and will always do her best to stir a tempest in a thimble.”

Ah!  That explains everything.

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

But then, Dr. Frances acknowledges some retrospective misgivings:

“But in retrospect, there are two things about the project I much regret. Firstly, it was very unwise to do guidelines with drug industry funding. Even though they were fairly done, accurately reported, and contained built in methodological protections against industry-favorable bias, the industry sponsorship by itself created an understandable appearance of possible bias that might reduce faith in the sound advice and useful method contained in them. It was an error in judgment on my part that I apologize for. I have learned from my mistake and hope others do as well.”

So, there was absolutely nothing wrong with the guidelines, but the acceptance of pharma money may have created an appearance of bias.  And although no such bias existed, Dr. Frances is apologizing for creating this appearance.  But remember the EKS commitment quoted earlier:  “We are also committed to helping Janssen succeed in its effort to increase its market share and visibility in the payor, provider, and consumer communities.”  This is a clear statement of  bias.  It’s not an appearance of bias; it’s not possible bias.  It is out and out, unmitigated bias.  They express commitment, not to some improvement in client outcomes or welfare, but to increasing Janssen’s market share.  Drs. Frances, Docherty, and Kahn were hired to market Risperdal.  They were well paid, and they delivered what their employer expected of them.

And incidentally, despite his misgivings, there’s no indication that Dr. Frances has refunded his share of the $900,000 from J & J.  “May one be pardon’d and retain the offence?” (Hamlet, Act 3, Scene 3)

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

“Secondly, I did not at the time anticipate, nor did the experts, that the atypical antipsychotics would be so frequent a cause of obesity and of the serious complications that follow from it. The considerable risks involved in using these new medications, and ways of avoiding these, were then unknown and not covered in the guideline.”

So, he assumed without evidence that the drug was safe unless proven dangerous, when in fact, good practice would be the opposite:  assume that the drug is dangerous, until it’s proven safe!  But, in any event, it wasn’t Dr. Frances’s fault.  After all, who could have known?


In 1996, the EKS’s Treatment of Schizophrenia guidelines were published as a 58-page supplement in The Journal of Clinical Psychiatry.  It’s an interesting document, and it certainly does promote the use of Risperdal (risperidone).  But of even more interest is this statement in the preface to the supplement .  It was written by Alan Gelenberg, MD, Editor in Chief of the journal.  Dr. Gelenberg begins the Preface with some words of praise for the guidelines, but also advocates caution with regards to pharma-funded projects:

“…in conditions such as bipolar disorder and schizophrenia, where the primary treatments are medications, industry is a looming presence.  Pharmaceutical companies devote enormous sums to academic departments and individual faculty members who consult, conduct research, and teach under the auspices of the company.  These then are the experts who create consensus guidelines.  While few of us sell our opinions to the highest bidder, fewer still are immune from financial influence.” [Emphasis added]

So Dr. Gelenberg could see these issues very clearly in 1996, when the guidelines were published; but Dr. Frances, despite his mea culpa in the Huffington Post last March, still hasn’t grasped the issue.  In that document, from which I quoted earlier, Dr. Frances contends that the guidelines “…contained built in methodological protections against industry-favorable bias…”.  But as Dr. Gelenberg so clearly points out, the expert consultants on whose opinions the guidelines were based were already subject to industry influence by the very fact of their status within the psychiatric community.  So, in fact, industry-favorable bias was actually built in.

Page 2 of the supplement lists the 87 expert psychiatrists on whose questionnaire responses the guidelines were based.  The list is in alphabetical order, and I checked the first fifteen names for links to pharma.  Two of the fifteen are deceased.  Of the remaining thirteen, nine have disclosed that they have received payments from pharmaceutical companies, and eight of these have received payments from Janssen Pharmaceutica/J & J.

I have no way of checking if these financial links were present in 1995/96 when the guidelines were produced, but the extent of these individuals’ involvement with pharma today suggest that Dr. Gelenberg’s concerns were probably well founded.

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

On the supplement’s sub-cover there is a brief acknowledgement of Janssen’s funding:

“This project was supported by an unrestricted educational grant from Janssen Pharmaceutica.”

The term “unrestricted” has a very specific meaning in this context.  It means that the recipients of the grant are not required to produce any particular result.  Essentially there is an expectation that both grantor and recipient will take steps to keep one another at arms’ length.  The term “unrestricted” is, in a sense, a warranty to the reader that the document in question is free from funder bias.

In the light of the material quoted above, it strikes me that the description “unrestricted” in this case was at best misleading, and possibly a blatant deception.


If Dr. Frances really wants to put this matter to rest, he needs to answer these questions publicly and unambiguously:

  1. Are the allegations against him and his EKS partners that are set out in detail in the David Rothman report accurate?
  1. Are the quotations in that report that are attributed to Dr. Frances accurate?

If the answer to both of these questions is No, then I suggest that Dr. Frances start devoting his time and energy to addressing these matters, and clearing his name, because the allegations are very serious.

But if the answer to one or both of these questions is Yes, then I respectfully suggest that Dr. Frances exit the stage with whatever dignity he can muster, and resume his well-earned retirement.


Mickey Nardo, MD, has also posted David Rothman’s report on his website, 1 Boring Old Man.  Dr. Nardo has also written a post on this topic.  The post is titled detestable.

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

I have quoted from David Rothman’s report in this post, but I’ve confined my attention to material concerning Dr. Frances and EKS.  In fact, the report covers a lot more ground, and gives a great deal of detail on the pharma-psychiatry corruption that has marred the landscape in this field for so long.  It’s well worth reading.

For instance, here’s an insightful little gem from page 21:

“Shon [Steven Shon MD, Medical Director of the Texas Department of Mental Health and Mental Retardation] was also considered a pivotal figure by another J&J employee, Percy Coard…After thanking his colleagues for attending a Shon presentation, he listed all the reasons why J&J wanted a ‘strategic alliance’ with him.  As Coard explained, Shon was a KOL [key opinion leader], influential in the public sector, where ’85 Percent of all anti-psychotic dollars come from;’ he has influenced and supported the use of new drugs in TMAP [Texas Medication Algorithm Project], and a proactive approach to him ‘to support/partner with his current and future projects in the public sector arena will continue to position Janssen as a true partner in public mental health initiatives.'”

Such a sense of civic responsibility!

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

Robert Whitaker discusses EKS and the Tri-University Guidelines in his latest book, Psychiatry Under the Influence, p 149-150.


And for anyone who has any doubts concerning the effectiveness of pharma-psychiatry’s marketing machine, here’s a graph produced by the Agency for Healthcare Research and Quality (AHRQ), a division of the US Department of Health and Human Services.

AHRQ fig 1 on antipsychotics

So between 1997 and 2007, total expenses for neuroleptic drugs in the US went from $1.7 billion (corrected to 2007 value) to $7.4 billion.  This is an increase of $5.7 billion over and above any increase due to inflation.

The cost of these extra sales in terms of reduced life expectancy and quality of life is psychiatry’s legacy to humanity.

Neuroleptic Drugs And Mortality

In November of last year, the Schizophrenia Bulletin published online a research study:  Antipsychotic Treatment and Mortality in Schizophrenia, by Minna Torniainen et al.  The research was conducted in Sweden.

The authors offer the following background for the study:

“It is generally believed that long-term use of antipsychotics increases mortality and, especially, the risk of cardiovascular death. However, there are no solid data to substantiate this view.”

and the following conclusions:

“Among patients with schizophrenia, the cumulative antipsychotic exposure displays a U-shaped curve for overall mortality, revealing the highest risk of death among those patients with no antipsychotic use. These results indicate that both excess overall and cardiovascular mortality in schizophrenia is attributable to other factors than antipsychotic treatment when used in adequate dosages.”

On the face of it, this finding would seem to upset the notion, widely accepted in antipsychiatry circles, that neuroleptic drugs are toxic, and that their use, especially prolonged use, markedly reduces life expectancy.  There are, however, some problems with the study that need to be considered.

First, let’s take a look at one of the graphs presented in the article.

Torniainen fig 1 upper half









Fig. 1.  (a) Overall mortality as hazard ratios in the chronic patient population (N = 21 492) compared with mortality in the control sample.

What we see graphed here are the mortality figures for the four groups identified and followed in the study.

  • participants with no exposure to neuroleptic drugs
  • those with low exposure
  • those with moderate exposure
  • those with high exposure

Mortality is presented as a hazard ratio compared to matched pairs in a control sample.

The actual numbers are:

Tornianen hazard ratio chart






So the individuals with no neuroleptic exposure had 6.3 times the death rate as their matched controls.  The low exposure group, 4.06, and so on.

The black vertical lines through each graph value represent the 95% confidence interval for that value.  What this means is that we can be 95% confident that the true value of each hazard ratio lies within the range of the vertical black line.  Note that the confidence interval is widest for the zero use group.  This is because they were numerically the smallest group.

The numbers of people who died in each group were:

Tornianen study Death rates





Total sample size was 21,492, and the results appear to confirm the authors’ conclusions: that the mortality rates for people “diagnosed with schizophrenia” bear a U-shaped relationship to neuroleptic use, with the highest rates associated with both zero and high use.

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

Note that two comparisons were made.  Firstly, all the individuals labeled schizophrenic were compared to the “control sample”, and secondly within the “schizophrenia” group comparisons were made between the four sub-groups:  zero, low, moderate, and high users of neuroleptic drugs.

For comparative research of this sort to be valid, there is a fundamental requirement that the target group has to be essentially similar to the comparison group in every respect, except the characteristic under study, which in this case is, firstly, the presence of a “diagnosis of schizophrenia,” and secondly, the degree of neuroleptic exposure.

The importance of this assumption can be readily appreciated by an example.  Suppose that all the members of the zero-neuroleptics group in this study had a history of heart problems, and none of those taking the drugs had such problems.  Clearly, the conclusion would be flawed because a group of people with heart problems will, other things being equal, have a higher mortality rate than people without such problems.

It is to counter such problems that researchers use double-blinded randomized controlled trials (DBRCT’s).  In a DBRCT, study participants are recruited, and are randomly assigned to receive either a treatment or a placebo.  The treatment provider, the client, and the person who is rating the outcome are “blinded” – i.e. they don’t know which participants have received the treatment and which have received the placebo.

The randomization process allows us to be reasonably, but not totally, certain that the two groups are sufficiently similar to allow comparisons to be made.

The study under consideration here was not a DBRCT.  It was an observational, matched pairs study.  Here’s how the authors describe their methods:

“We identified all individuals in Sweden with schizophrenia diagnoses before year 2006 (N = 21 492), aged 17–65 years, and persons with first-episode schizophrenia during the follow-up 2006–2010 (N = 1230). Patient information was prospectively collected through nationwide registers.  Total and cause-specific mortalities were calculated as a function of cumulative antipsychotic exposure from January 2006 to December 2010.”

The study is observational in that the authors simply identified all individuals in Sweden with “schizophrenia diagnoses” prior to 2006 and individuals who had a first-episode of psychosis and a “diagnosis of schizophrenia” between 2006 and 2010.  They then searched death registers and drug prescription registers to observe and document mortality rates for zero, low, moderate, and high users of neuroleptic drugs.

As mentioned earlier, the study entailed two different comparisons – mortality rates for individuals labeled “with schizophrenia” were compared to rates for the control sample; and within the “schizophrenia” groups mortality rates were compared for zero, low, moderate, and high neuroleptic users.

The control groups for the first comparison consisted of  “…age- and gender-matched controls from the general population…”

“The mortality in persons with schizophrenia was compared with a control sample from the general population.  For each person with schizophrenia, we identified 10 age- and sex-matched persons without schizophrenia.”

The results for the first comparison were:

Tornianen first comparison.

The authors don’t tell us exactly how the matched controls were selected.  All we know is that for each member of the “schizophrenia” group there were ten controls of the same age and gender who did not “have schizophrenia”.  This was a total of 214,670 individuals.

There are two problems with this approach.  Firstly, no amount of matching of this sort can produce truly comparable groups.  The reader has only to bring to mind people of the same age and gender as him/herself to realize that the differences will outweigh the similarities.  Using ten controls for each study participant does improve the situation somewhat, in that the resulting averaging will tend to smooth out extreme differences, but the problem is by no means eliminated.

Secondly, “schizophrenia” is a notoriously unreliable label.  The DSM-5 trials yielded Kappa scores of only 0.46.  What this means essentially is that, of the 21,492 participants labeled as “having schizophrenia”, a substantial number would not be so labeled if examined by an independent psychiatrist.

Matched-pairs studies can be useful in general medicine, where the number and the nature of confounding variables are often relatively limited.  But they are problematic in psychological/behavioral research because of the inherent complexity of the subject matter and the almost infinite range of potential confounders.


As mentioned earlier, the graph and the hazard ratios would appear to confirm the authors’ conclusion that the zero-users had the highest mortality rate.  However, there are a number of observations that need to be made.

1.  There is normally a great deal of pressure on people who receive “a diagnosis of schizophrenia” to take neuroleptic drugs. From the numbers presented in the study, 2077 of the 21,492 participants took no neuroleptics.  So, either the treating psychiatrists did not prescribe the drugs, or the individuals refused to take them.  In either event, I think it is clear that these individuals, taken as a group, are dissimilar from those individuals who did take the drugs.  In the absence of more detailed information about these individuals, it is not safe to attribute their excess mortality to the fact that they didn’t take the neuroleptics.  Indeed, the authors acknowledge this:

“Because the nature of this study is observational, the associations may not necessarily mean causality. The results concerning comparative mortality between different exposure groups did not change substantially when the clinical and sociodemographic characteristics were controlled in the secondary analysis within the patient population. However, it is not possible to fully adjust for the severity of the illness and lifestyle characteristics by using such databases, which do not include information on smoking or diet, for example. Disease may be more severe in patients with high medication use than in patients with moderate antipsychotic use, and therefore the higher mortality in this group may partially derive from disease severity.”

But, by exactly the same token, some unidentified extraneous factor may be at work within the zero-use group and may account for their higher mortality rate.

2.  The zero-use individuals may not have been truly zero-use.

“…because antipsychotic medications that may be used in hospitals are not recorded in the Prescribed Drug Register.”

“…no information was available on the use of medication during the hospital treatment days…”

3.  The finding that “the highest overall mortality was observed among patients with low antipsychotic exposure…” is an over-simplification.  In fact, some of these individuals had a particularly low hazard ratio, while others had a particularly high  hazard ratio.  This can be seen clearly in Table 3:

Torniainen Table 3

In this table the moderate use group is used as the reference point.  This is why all the hazard ratios for that group are 1.  Hazard ratios for the other exposure groups are calculated as compared to the moderate group.

Here again, we see (top line) that the highest overall hazard ratio is for the zero-use group (1.56); next the high-exposure group (1.43); then the low-exposure group (0.97).  The actual numbers differ from the earlier hazard ratios because those were calculated in reference to the matched controls, whereas the ratios in Table 3 are calculated in reference to the moderate-use group

Although the authors were unable to obtain information on drug prescriptions during hospital stays, they were able to determine whether a participant had been hospitalized and when.  This is why they were able to calculate the hazard ratios for individuals who had had inpatient treatment prior to the follow-up period.  Note that the hazard ratios for zero-users who had had previous inpatient treatment are high:  3.46 for people who had had treatment within the year prior to follow-up and 1.69 for those who had inpatient treatment earlier.  And also note that the hazard ratio for the zero-users who had had no treatment, but were identified only from disability pension rolls, is relatively low:  1.06.  The hazard ratio for the high users in the same category is 2.19.  So the authors’ conclusion that the highest risk of death was “among those patients with no antipsychotic use”, is not the whole truth.  The group with the highest risk consists of those individuals who had zero exposure to the drugs and who had had inpatient treatment within the previous year.  The zero exposure individuals who had no record of formal treatment had a much lower risk ratio (1.06).  This, of course, doesn’t prove that treatment is causing excess mortality, but it is at least as noteworthy as the U-shaped curve highlighted in the authors’ conclusion.

4.  As indicated earlier, it is widely accepted that prolonged use of neuroleptic drugs reduces life expectancy, and that these toxic effects continue to impact mortality rates as long as the individual continues to take the drugs. To adequately monitor and study this effect, it is, I suggest, particularly important to include older people in the research.  In this study, however, only individuals below the age of 65 were included.  This will almost certainly have the effect of artificially lowering the mortality rate for the neuroleptic users.  The senior years are precisely the time when one would expect to see the toxic effects of a drug become most evident.  The authors provide no rationale for setting this upper age-limit.

5.  The total number of deaths in this study was 1591. Causes of death were given as follows:

Tornianen causes of death charge





This leaves 483 deaths unaccounted for.  The authors tell us how the 1,108 deaths break down by exposure category, but we are given no information on the other 483 deaths.  This is 30% of the total.  We don’t know how these people died, nor how their deaths were distributed among the four exposure groups.

I wrote to Jari Tiihonen, the correspondence author, for information on this matter.  In his reply, Dr. Tiihonen stated that this information was not available.  It is possible that the 483 “missing” deaths were distributed across a large number of relatively low frequency causes.  Studies of this kind often use an “Other Cause” category to capture this information.  The complete absence of information on these deaths in this study, however, is noteworthy.

6.  Perhaps the most serious problem with the study lies in the method that was used to define the four exposure groups. Let’s go back to a statement made in the “methods” section of the abstract:

“Total and cause-specific mortalities were calculated as a function of cumulative antipsychotic exposure from January 2006 to December 2010.”

My initial interpretation of this sentence, and I think it’s the interpretation that most people would make, is that mortalities were calculated during the follow-up period 2006-2010, and these mortalities were compared to lifetime cumulative drug exposure.  In fact, as becomes clear later in the text, this is not what was done.

“The identified schizophrenia patients were categorized into 4 DDD groups; (1) no antipsychotics during the follow-up, (2) small doses of antipsychotics or occasional use (0 DDD/ day–0.5 DDD/day, noninclusive), (3) moderate doses of antipsychotics (0.5 DDD/day–1.5 DDD/day, inclusive), and (4) high antipsychotic doses (>1.5 DDD/day).” [Emphasis added]

So the individuals in the study were categorized – not by cumulative lifetime exposure to neuroleptics, but only by exposure during the five-year follow-up period.  For example, a person who had been taking neuroleptics for decades, and came off the drugs in December 2005, and died in January 2006, would have been recorded as a mortality in the zero neuroleptic exposure group.

The phrase “cumulative antipsychotic exposure”, which occurs five times in the article, suggests lifetime exposure, and in my view the authors did not adequately emphasize the fact that the exposure data was actually limited to a five-year period.  This strikes me as particularly pertinent, in that it is precisely the long-term cumulative exposure to these drugs that is the primary cause of the mortality concerns.  The fact is that the present study provides no information on the effects of cumulative lifetime exposure to neuroleptic drugs.


Here’s a copy of the authors’ Figure 2.

Torniainen Fig 2

Fig. 2.  Mortality expressed as hazard ratios due to specific causes in patients with schizophrenia compared with the control sample.

The mortality figures for respiratory illnesses show a generally upward progression from zero-use to high use.  Figures for the other causes of death (cardiovascular, neoplasms, and suicide) show zero-use higher, or nearly as high, as high-use.  But look at the scales on the left of each figure.  The respiratory scale, which shows the neuroleptics in the worst light, is the tightest, and the cardiovascular scale, which shows zero use in the worst light, is the loosest.  Here’s what the data looks like when all causes of death are graphed on the same figure and on the same scale.

Tornianen Mortality composite change data

As can be seen, the U-shape becomes a good deal less evident.  The neoplasm line is fairly flat.  The death rate for respiratory illnesses is increasing markedly with increased drug use.  The suicide rate is sloping in the opposite direction.  Only the cardiovascular line is identifiably U-shaped:  a finding for which I can suggest no particular explanation, though it does seem unlikely that it reflects a lack of neuroleptic drugs.  More likely, it reflects the fact that the zero use group were not really zero use.


The conclusions from the abstract were quoted earlier, but there is a more detailed conclusions section in the text of the article.

“Patients with low or moderate antipsychotic exposure have substantially lower overall and cardiovascular mortality than patients with no exposure or high exposure, which clearly indicates that both excess overall and cardiovascular mortality in schizophrenia is attributable to other factors than long-term antipsychotic treatment when used in adequate dosages. An alarmingly high excess mortality among first-episode patients who do not use any antipsychotics deserves more attention, in order to increase adherence to their prescribed pharmacological treatment. Despite the importance of nonadherence, clinicians spend too little time on addressing this issue. For example, long-acting antipsychotic injections (LAIs) are associated with about 60% lower all-cause discontinuation than corresponding oral formulations among first-episode patients.  Thus, more use of LAIs might result in substantially lower excess mortality.  Focusing more attention particularly on first-episode and recently hospitalized patients who are not using any antipsychotics, and on patients with antipsychotic doses higher than 1.5 DDD/day, is essentially important in the prevention of premature death in people with schizophrenia.”

And there it is:  people who don’t use the drugs have higher mortality, so steps must be taken to ensure adherence.  And this conclusion is being promoted even though the identification of individuals with zero cumulative exposure was seriously flawed and unreliable.


The final author listed in the article is Jari Tiihonen.  Dr. Tiihonen works for the Department of Mental Health and Substance Abuse Services in Finland; the Department of Clinical Neuroscience, Karolinska Institutet, Sweden; and is Professor and Chairman, Department of Forensic Psychiatry, University of Eastern Finland.

Though he is not identified as such, it is fairly clear that Dr. Tiihonen is the senior investigator in the present study.  He is identified as the correspondence author, and he is the Team Leader of the Center for Psychiatric Research at the Karolinska Institutet.

In the present paper it is acknowledged:

“In the last 3 years J.T. [Jari Tiihonen] reports serving as a consultant to Lundbeck, Organon, Janssen-Cilag, Eli Lilly, AstraZeneca, F. Hoffman-La Roche, and Bristol-Myers Squibb; he has also received fees for giving expert opinions to Bristol-Myers Squibb and GlaxoSmithKline, and lecture fees from Janssen-Cilag, Bristol-Myers Squibb, Eli Lilly, Pfizer, Lundbeck, GlaxoSmithKline, AstraZeneca, and Novartis; he is also a member on the advisory board of AstraZeneca, Janssen-Cilag, and Otsuka, and he has received a grant from the Stanley Foundation.”


The article didn’t attract a great deal of attention.  But I did find three interesting citations.

Joel Yager, MD, psychiatrist, writing in the NEJM Journal Watch wrote:

“Even though this observational study cannot prove causality, the notably higher mortality among patients with no antipsychotic exposure suggests that adherence-increasing interventions, including use of long-acting injectable medications, might reduce risk for death.” [Emphasis added]

And schizophrenia.com:

Antipsychotic Treatment and Mortality in Schizophrenia: No Drugs = Higher Mortality

And Joanna Lyford writing on Medwire News:

“The relationship between antipsychotic use and mortality in people with schizophrenia shows a clear U-shape curve, with the highest risk of death seen in those with no antipsychotic exposure, a Swedish cohort study has found.” [Emphasis added]

None of the articles mentioned the fact that the results applied only to those individuals who had received prior treatment (particularly inpatient treatment), and was not evident at all in people with no record of treatment.  Nor did any of the articles mention the fact that the “cumulative antipsychotic exposure” applied only to the five-year follow-up period, and that neuroleptic use prior to that period was not considered.

Psychiatric Diagnoses:  Labels, Not Explanations

On March 16, Ronald Pies, MD, published an article in the Psychiatric Times.  The article is titled The War on Psychiatric Diagnosis, and the sub-title synopsis on the pdf version reads:  “A recent report that argues against descriptive diagnosis in medicine is historically ill-informed and medically naive, in the opinion of this psychiatrist.”

Dr. Pies is a very prestigious and eminent psychiatrist.  He is a professor of psychiatry at both Syracuse and Tufts.  He was the first editor of Psychiatric Times, which, by its own account, provides “News, Special Reports, and clinical content related to psychiatry” for “…psychiatrists and allied mental health professionals who treat mental disorders…Circulation of the monthly print publication is approximately 40,000.”

The report that Dr. Pies considers “historically ill-informed and medically naïve”, is the BPS November 2014 paper Understanding Psychosis and Schizophrenia, which has been widely discussed in recent weeks.

. . . . . . . . . . . . . . . . 

There is much in Dr. Pies’ paper that warrants critical examination, but I would like to focus here on just one topic:  the explanatory value of diagnoses.

Dr. Pies himself acknowledges the centrality of this matter, and writes:

“But there is a larger issue raised in the BPS report that goes to the very heart of psychiatric diagnosis, which the report tries to discredit with the following argument:

We normally expect medical diagnoses to tell us something about what has caused a certain problem, what the person can expect in future (‘prognosis’) and what is likely to help. However, this is not the case with mental health ‘diagnoses,’ which rather than being explanations are just ways of categorizing experiences based on what people tell clinicians. . . . For example, someone who says that they are hearing voices might be given a diagnosis of schizophrenia. Since this says nothing about cause, it makes little sense to say that the person hears the voices ‘because of ‘ the schizophrenia.

Actually, it makes a good deal of sense, in precisely the same way it makes sense to say, ‘Mr Jones has severe facial pain because he has tic douloureux;’ or ‘Smith has severe left-sided head pain and nausea because he has migraines.’ We still do not know the precise causes of these conditions; moreover, the diagnosis of  tic douloureux (literally, ‘painful tic’) or migraine headache (etymologically, headache ‘in half the cranium’) is made almost entirely on the basis of ‘what people tell clinicians’—not on the basis of an abnormal laboratory value, x-ray film, or anatomical finding. (Of course, certain tests, such as a CT scan of the head, can help rule out other diagnostic possibilities, such as a brain tumor.)”

The essence of Dr. Pies’ contention here is that psychiatric diagnoses are just as valid as diagnoses in general medicine, and that, in particular, the absence of knowledge concerning causes does not diminish their status or usefulness.

It has long been my contention that psychiatric “diagnoses” have no explanatory value, and in fact constitute nothing more than vague, unreliable re-labeling of the presenting problems.

This is clearly demonstrated in the hypothetical conversation:

Client’s parent:  Why is my son so paranoid?  Why does he just sit in his room all day?  Why won’t he do anything?

Psychiatrist:  Because he has an illness called schizophrenia.

Parent:  How do you know he has this illness?

Psychiatrist:  Because he is so paranoid, sits in his room all day, and won’t do anything.

The only evidence, and I stress the only evidence, for the so-called illness is the very behavior that it purports to explain.  The psychiatric explanation essentially comes down to:  he is paranoid, sits in his room all day, and won’t do anything, because he’s paranoid, sits in his room all day, and won’t do anything.  There is nothing more to it than that.

I realize that I’ve labored this matter to the point of tedium. But I’ve done so for two reasons.  Firstly, because it is one of the core flaws in psychiatry.  Its diagnoses have no explanatory value.  They are nothing more than labels.  Secondly, because psychiatry consistently fails to respond to this particular criticism, and with equal consistency presents these labels as if they did have explanatory value.

The present article by Dr. Pies is a perfect example of the second point, because although Dr. Pies appears to address the issue, he actually side-steps it.

Let’s go back to the quote from the BPS article.

We normally expect medical diagnoses to tell us something about what has caused a certain problem…

This is absolutely accurate.  When a person consults a physician concerning a medical problem or concern, there is a general expectation that the diagnosis, if forthcoming, will provide an explanation of the problem.  And in practice, this is normally the case.  If a person reports exhaustion, pulmonary congestion, elevated temperature, pain in the chest, and nasty-looking phlegm, his diagnosis might be pneumonia.  Pneumonia is a viral or bacterial infection of the lung tissue.

What is noteworthy here, in the present context, is that we have two distinct elements:  the symptoms and the cause of the symptoms.  The person consults a physician because of the symptoms, and, from the physician, he learns the cause of these symptoms.  This is what diagnosis means:  determining the cause and nature of a pathological condition.  Wikipedia gives the following definition:

“Medical diagnosis…is the process of determining which disease or condition explains a person’s symptoms and signs.” [Emphasis added]

Another critical factor in this issue is that there has to be a clear logical link between the symptoms and the diagnosis.  If, for instance, the physician’s diagnosis in the above scenario were “incorrect curvature of the spine”, there would, I suggest, be an enormous burden of proof as to how this particular pathology could cause these particular symptoms.  But with a diagnosis of pneumonia, the logical link is clear:  the infection causes exudation of blood and other fluid into the lung tissue; the immune system triggers an increase in temperature, etc..

So let’s see how our consultation conversation might run in this case.

Patient:  Why am I so tired; why did my temperature spike; why am I spitting up such dreadful-looking phlegm?

Physician:  Because you have pneumonia.

Patient:  How do you know I have pneumonia?

Physician:  Because I can hear characteristic sounds through the stethoscope; your chest X-ray shows large quantities of fluid in both lungs; your sputum labs are positive for pneumococcus; and because everything you have told me is consistent with this diagnosis.  I can show you the X-rays if you like.

The difference between this kind of conversation and the psychiatric conversation is obvious.  In the pneumonia case, the physician has progressed from the symptoms to the essential underlying nature of the illness.  In psychiatry, no such progress has occurred or can occur.  In psychiatry, the so-called symptoms are the essence of the problem.  There is no underlying reality to which the symptoms point.  The “symptoms” and the “illness” are identical.

Back to the BPS quote:

“For example, someone who says that they are hearing voices might be given a diagnosis of schizophrenia. Since this says nothing about cause, it makes little sense to say that the person hears the voices ‘because of ‘ the schizophrenia.”

Again, this is accurate.  “Schizophrenia” is a label, not an underlying explanatory entity that enables us to understand the symptoms.  The phrase  “…because he has schizophrenia” is a form of words that looks like an explanation, but in fact isn’t.

To illustrate this, let’s consider another example.  Imagine a small child running tearfully to his mother with the complaint that another child has been hitting him.  Mother gathers the victim to her arms and soothes him.

Mother:  It’s OK.  I’ve got you.  It’s OK. etc.

Child:  Why does he keep hitting me?

Mother:  Because he’s a bully.  Don’t mind him.

The phrase “because he’s bully” looks like an explanation, and will be accepted by the child as an explanation, but in fact it has no explanatory value.  All we have to do to see this is ask the question:  “How do you know he’s a bully?”, and the only possible answer is “because he keeps hitting you”.

The statement “he beats you because he is a bully” is logically equivalent to the statement:  “He beats you because he beats you.”  It contains no explanatory insights into the aggressor’s action.  And psychiatric explanations are exactly of this kind.

Now, please don’t misunderstand me.  This is not a logical critique of mothers who try to comfort their children.  As parents, we do what we can to comfort our children, and there is no great onus with regards to logic or science.  But psychiatric concepts and assertions do need to pass the tests of logic and science.

The statement:  “Your son hears voices because he has schizophrenia” is logically equivalent to “Your son hears voices because he hears voices.”  Schizophrenia is nothing more than the label that psychiatry gives to that loose cluster of vaguely defined thoughts, feelings, and/or behaviors that are listed on page 99 of DSM-5.  These are:

  1. Delusions
  2. Hallucinations.
  3. Disorganized speech (e.g., frequent derailment or incoherence).
  4. Grossly disorganized or catatonic behavior.
  5. Negative symptoms (i.e., diminished emotional expression or avolition)

The simple fact of the matter is that the reasons underlying these thoughts, feelings, and behaviors are as varied as the individuals who experience them.  But psychiatrists make no attempt to explore these reasons.  Instead, they rely on the medical-sounding, but facile,  “because-he-has-schizophrenia” form of words.  As in so many areas, psychiatry has become intoxicated by its own rhetoric, and individual practitioners seem to believe that this form of words actually has some explanatory value.

Back to Dr. Pies:

“Actually, it makes a good deal of sense, in precisely the same way it makes sense to say, ‘Mr Jones has severe facial pain because he has tic douloureux;’ or ‘Smith has severe left-sided head pain and nausea because he has migraines.’  We still do not know the precise causes of these conditions; moreover, the diagnosis of  tic douloureux (literally, ‘painful tic’) or migraine headache (etymologically, headache ‘in half the cranium’) is made almost entirely on the basis of ‘what people tell clinicians’—not on the basis of an abnormal laboratory value, x-ray film, or anatomical finding.”

So there is a fairly profound disagreement.  The BPS say that the explanation “because he has schizophrenia” makes little sense.  Dr. Pies says it makes a good deal of sense. Let’s take a closer look.  First, let’s go back to the BPS statement which Dr. Pies quoted and which I reproduced above.  Although there are no quotation marks around this passage, it is actually a verbatim quote from the BPS paper, but a crucial piece of the quote has been omitted.  (The omission is indicated by an ellipsis in the regular online version, but there is no ellipsis in the pdf version.)

The omitted passage is:

“The Diagnostic and Statistical Manual of the American Psychiatric Association (DSM) explicitly states that its categories say nothing about cause – in its own words it is ‘neutral with respect to theories of aetiology’.”

So a summary of the BPS passage might look something like this:

  1. medical diagnoses give us the cause or explanation of a problem
  2. psychiatric diagnoses, by contrast, do not give causes or explanations
  3. psychiatric diagnoses are just ways of categorizing clients’ reports
  4. the APA acknowledges that its diagnoses say nothing about cause
  5. therefore the label schizophrenia has no explanatory value
  6. so, to say that a person hears voices because he has schizophrenia makes little sense

What Dr. Pies has omitted is item 4 arguably the most important part of the passage.  So Dr. Pies is accusing the BPS of leaping from

psychiatric diagnoses are just ways of categorizing clients’ reports


therefore the label schizophrenia has no explanatory value

and ignores the interim premise which is crucial to the issue.  Dr. Pies then uses this distortion to make the point that some diagnoses in general medicine are based entirely on patient report but are nevertheless considered valid and useful.  This, of course, is non-contentious.  There are, indeed, genuine medical conditions which are diagnosed largely on the basis of patient report. Dr. Pies mentions tic douloureux as an example, and states that the precise cause of this illness is unknown. But he is, I suggest, being less than candid, because a great deal is known, and has been known for decades, about the cause of tic douloureux, which, incidentally, is now usually called trigeminal neuralgia.  Here’s the entry for this illness in the 1963 edition of Taber’s Cyclopedic Medical Dictionary:

“Degeneration of or pressure on the trigeminal nerve, resulting in neuralgia of that nerve…The pain is excruciating.  Usually occurs after forty.  Pain is paroxysmal, radiating from angle of the jaw along one of the involved branches.  If the first branch, a shocklike pain is felt along the eye and back over the forehead.  If it is the middle fiber, the upper lip, nose, and cheek under the eye are affected.  If it is the third branch, pain is in the lower lip and outer border of tongue on affected side.  Pain is momentary but returns again and again.” (p T-30)

More up-to-date information is provided by drugs.com, a service of Harvard Health Publications:

“In some cases, the cause of trigeminal neuralgia is unknown. In many people, however, something seems to be irritating the trigeminal nerve, usually in the area of the nerve’s origin deep within the skull. In most cases, the irritation is believed to be caused by an abnormal blood vessel pressing on the nerve. Less often, the nerve is being irritated by a tumor in the brain or nerves. Sometimes, the problem is related to a rare type of stroke. In addition, up to 8% of patients who have multiple sclerosis (MS) eventually develop trigeminal neuralgia as a result of MS-related nerve damage.”

So, if a patient were to ask his physician why he is experiencing excruciating stabbing pains in his face, the response “because you have tic douloureux” is a perfectly logical explanation.  It might, or might not, be correct – that is not the issue.  But it is a coherent, valid explanation, and is not simply a relabeling of the presenting problems, which is  the essential status of all psychiatric diagnoses, other than those specified as being “due to a general medical condition”.

What’s particularly interesting here is that the BPS document is in fact very clear on this matter.  The sentence following the passage quoted by Dr. Pies reads:

“An analogy with physical medicine might be a label such as ‘idiopathic pain’, which merely means that a person is reporting pain, but a cause of that pain cannot be identified.”

Idiopathic means “of unknown cause, as a disease.”  (Random House Webster’s College Dictionary, 1992).  So if a patient were to ask a physician why he was experiencing severe facial pain, the response “because you have idiopathic pain” would simply be a restatement of the presenting problem, and would have no explanatory value.  The point being made in the BPS report is that a relabeling of the presenting problem that entails no understanding of cause has no explanatory value.  The phrase “because you have schizophrenia” is precisely on a par, logically, with “because you have idiopathic pain.”  Dr. Pies’ introduction of, and comparison to, “because you have tic douloureux” is an enormous red herring.  His use of the etymological annotation “painful tic” is also a red herring, in that etymology is a poor guide to current meaning.  The etymology of the word “mortgage”, for instance, is “death pledge”, because the original meaning of a mortgage was a pledge that a debt would be repaid from one’s estate after one’s death.  This is interesting, of course, but has no relevance to the current meaning of the term.

Certainly there are disease entities that general medicine has named, and can identify with reasonable accuracy, prior to establishing the etiology or cause of these illnesses.  But this is fundamentally different to the situation that prevails in psychiatry.  Firstly, in general medicine there are always prima facie reasons for believing that the condition is an organic pathology.  Secondly, the quest of general medicine for explanations and causes has been remarkably successful.

Neither of these conditions exists in psychiatry.  In fact, despite an enormous amount of highly motivated research in this area, no psychiatric “illness” has ever been reliably established to be the result of a specific neural pathology.  Even Thomas Insel, MD, Director of NIMH, wrote on April 29, 2013:

“While DSM has been described as a ‘Bible’ for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been ‘reliability’ – each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment.”

Whilst I don’t agree with Dr. Insel in all areas, on this matter he has hit the nail squarely on the head.

The bottom line is this:  if one doesn’t know the cause of something, then one can’t explain it.  Explanation is the presentation of causes.  And despite their frequent claims to the contrary, psychiatrists do not know the cause of the loose collection of thoughts, feelings, and/or behaviors that they call schizophrenia.  They assume that any decade now they will discover this cause in the form of some neural pathology.  Meanwhile, they go on telling their clients the falsehood that they have chemical imbalances, or neural circuitry anomalies or whatever is the latest fashion, and that these putative illnesses can be corrected by drugs or electric shocks to the brain.  And they ignore the reality:  that the best (indeed only) way to understand people is to talk to them patiently, compassionately, and with humility, and without the assumption that one already knows the source of their troubles.  It is only in this way that we discover that people’s so-called symptoms are understandable within the context of each person’s unique history and current circumstances, and that the facile labels cataloged so conveniently by the APA are an irrelevant travesty.

And, indeed, Dr. Pies himself, even though he clings tenaciously to the need for psychiatric “diagnoses”, acknowledges the additional need to take the time to get to know clients:

“Finally, while diagnosis is a necessary first step in helping the patient with emotional, cognitive, or behavioral problems, it is far from sufficient. We must enter empathically into the patient’s ‘inner world,’ and provide a safe, trustworthy environment for the exploration of the patient’s troubles. This takes time—it can’t be done in 15 minutes!—and it requires what psychoanalyst Theodor Reik eloquently called, ‘listening with the third ear.’ “

But what Dr. Pies neglects to add is that the 15-minute med check has become standard practice in psychiatric care.  Douglas Mossman, MD, Professor of Psychiatry at the University of Cincinnati, has written unambiguously:

“Even psychiatrists who deplore 15-minute med checks recognize that they have become standard care in psychiatry.”

Glen Gabbard, MD, a widely published professor of psychiatry at Baylor and Syracuse, has written on Psychiatric Times:

“There can be little doubt in our current era that the brief ‘med check’ is becoming standard practice in psychiatry.”

Dr. Pies himself, in an earlier paper (Psychiatrists, Physicians, and the Prescriptive Bond) has written:

“Unfortunately, many prescriptions for psychotropics are written in haste—often after the infamous ’15-minute med check’ – and without any real understanding of the patient’s inner life or psychopathology.”

Dr. Pies, incidentally, also failed to mention that Theodor Reik (1888-1969) was a psychologist, not a psychiatrist, and in fact, had to fight a lawsuit against the medical community in order to establish the principle that psychoanalysis could be practiced by non-physicians.

Nor does Dr. Pies seem to recognize that psychiatry’s contention, that the DSM entities are bona fide illnesses, is, in fact, the primary driving force behind the cursory treatment which he decries so ardently.  After all, if people’s problems are caused by brain malfunctions, and if psychiatric drugs correct these malfunctions, what need is there for dialogue or understanding?

There is no factual or logical evidence that the loose collection of vaguely defined thoughts, feelings, and/or behaviors that psychiatrists call schizophrenia is a coherent entity, much less an illness.  Nevertheless, psychiatrists continue, not only to make this groundless assertion, but also to prescribe neurotoxic chemicals to “treat” this pseudo-illness, often against the vehemently expressed wishes of the victims.  This is not the practice of medicine.  It is a travesty which no amount of Dr. Pies’ sophistry can mitigate.

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

With regards to the title of his piece –  The War on Psychiatric Diagnosis – Dr. Pies has this to say:

“If ‘war’ seems a somewhat overheated term in the title of this piece, I would recommend perusal of some of the anti-psychiatry Web sites, on which the ritual evisceration of psychiatry and psychiatrists is unapologetic and unrelenting.*”

The asterisk refers to a footnote:

“*In my view, the Web site of ‘Mad in America’ is particularly abusive toward psychiatrists, though it is far from the worst of the bunch”

Well, of course, there’s anger and vitriol on both sides of this issue, though I must say that MIA has always struck me as the epitome of civility and restraint.  But it’s important in this, as in any human endeavor, to rise above the rhetoric, and deal honestly and squarely with the issues.  And the issue on the table here is that psychiatric diagnoses – other than those clearly identified as “due to a general medical condition” – have no explanatory value, but are routinely and deceptively presented by psychiatrists as if they did.

And, Dr. Pies has not addressed that issue. 

Psychiatry is under criticism because its concepts are spurious, and its treatments are destructive.  The problems that psychiatry guards tenaciously as its turf are not medical in nature, but for the sake of that turf, are shoe-horned shamelessly into psychiatry’s bogus nomenclature, and are “treated” with neurotoxic drugs and electric shocks to the brain.  Petulant complaining about the “ritual evisceration of psychiatry and psychiatrists”, is no substitute for rational, honest, and informed debate.

The Dopamine Hypothesis of Schizophrenia – Version III

On November 27, 2014, the Division of Clinical Psychology of the British Psychological Society published a paper titled Understanding Psychosis and SchizophreniaThe paper was edited by Anne Cooke of Canterbury Christ Church University.  The central theme of the paper is that the condition known as psychosis is better understood as a response to adverse life events rather than as a symptom of neurological pathology.

The paper was wide ranging and insightful, and, predictably, drew support from most of us on this side of the issue and criticism from psychiatry.  Section 12 of the paper is headed “Medication” and under the subheading “Key Points”, you’ll find this quote:

“[Antipsychotic] drugs appear to have a general rather than a specific effect: there is little evidence that they are correcting an underlying biochemical abnormality.”

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

On the same date, The Mental Elf published a critique of the BPS paper.  The Mental Elf is an Internet website that purports to offer “reliable mental health research, policy, and guidance.”

The critique of the BPS paper is presented in three parts.  The first was written by Keith Laws, a psychologist, the second by Alex Langford, a trainee psychiatrist, and the third by Samei Huda, a consultant psychiatrist.

My purpose in writing this post is to address a paragraph in Dr. Langford’s essay.

“The ‘key point’ that there is ‘little evidence that [medications correct] an underlying abnormality’ is bizarrely unfounded. An excellent summary by Kapur & Howes (referenced earlier in the report itself) and further imaging studies by Howes and others provide solid evidence for elevated presynaptic dopamine levels being a key abnormality in psychosis, and there is copious evidence that inhibiting the action of this excess dopamine using antipsychotics leads to clinical improvement in psychosis.” [Emphasis added]

Note the term “bizarrely unfounded.”  Not “questionable”; not “misleading”; not “false”; not “overstated”; not “open to discussion”; not “unlikely” – but “bizarrely unfounded”!

In support of this assertion, Dr. Langford cites Oliver Howes and Shitij Kapur’s The Dopamine Hypothesis of Schizophrenia: Version III—The Final Common Pathway, Schizophrenia Bulletin, March 2009, which he claims provides “solid evidence” that elevated presynaptic dopamine levels are a “key abnormality in psychosis.”

To help put Dr. Langford’s assertion in perspective, here are some quotes from the Howes and Kapur article, interspersed with my comments.

“The dopamine hypothesis of schizophrenia has been one of the most enduring ideas in psychiatry.”

The authors describe how the dopamine hypothesis, which, incidentally, has been around since the late 60’s, has gone through two major revisions.  They refer to these as version I and version II.  Then:

“Since version II, there have been over 6700 articles about dopamine and schizophrenia. We selectively review these data to provide an overview of the 5 critical streams of new evidence: neurochemical imaging studies, genetic evidence, findings on environmental risk factors, research into the extended phenotype, and animal studies.”

“It [The Dopamine Hypothesis of Schizophrenia – Version III] explains how a complex array of pathological, positron emission tomography, magnetic resonance imaging, and other findings, such as frontotemporal structural and functional abnormalities and cognitive impairments, may converge neurochemically to cause psychosis through aberrant salience and lead to a diagnosis of schizophrenia.” [Emphasis added]

Note the word “may”, which suggests that the authors themselves did not regard the evidence as being quite as “solid” as Dr. Langford asserted.

“Although it is not possible to measure dopamine levels directly in humans, techniques have been developed that provide indirect indices of dopamine synthesis and release and putative synaptic dopamine levels.”

The fact that the primary variables cannot be directly measured, but rather are estimated from “indirect indices” suggests further that the evidence for version III may not be quite as solid as Dr. Langford asserts.

“Seven out of 9 studies in patients with schizophrenia using this technique have reported elevated presynaptic striatal dopamine synthesis capacity in schizophrenia, with effect sizes in these studies ranging from 0.63 to 1.89.”

“This, then, is the single most widely replicated brain dopaminergic abnormality in schizophrenia, and the evidence indicates the effect size is moderate to large.”

So essentially what’s being asserted here is that there is replicated evidence of abnormally high presynaptic dopamine production in the striatum area of the brain in people who carry a “diagnosis of schizophrenia.”

I don’t have the time to review all seven of the articles cited, but I did take a look at one:  Howes OD, Montgomery AJ, Asselin MC, et al. Elevated striatal dopamine function linked to prodromal signs of schizophrenia, Arch Gen Psychiatry. 2008 (number 20 in the reference list).  I chose this because the full text was readily available and because the principal author, Oliver Howes, MD, is also the principal author of the article cited by Dr. Langford.

Howes, Montgomery, Asselin, et al offer the following context for their study and report:

“A major limitation on the development of biomarkers and novel interventions for schizophrenia is that its pathogenesis is unknown.  Although elevated striatal dopamine activity is thought to be fundamental to schizophrenia, it is unclear when this neurochemical abnormality develops in relation to the onset of illness and how this relates to the symptoms and neurocognitive impairment seen in individuals with prodromal symptoms of schizophrenia..”

To address this question, they recruited three groups of people:

  • 24 “patients having prodromal symptoms of schizophrenia,” recruited from a community mental health center;
  • 7 “patients having schizophrenia” recruited from the same center;
  • 12 “matched healthy control subjects” from the same geographic area.

All of these individuals received an intravenous injection of 150 MBq (megabecquerels) of 18 F-dopa  30 seconds after the start of PET imaging which lasted for 95 minutes.  The neurochemistry of all this is extremely complicated, but the basic picture is this.  Dopa is an amino acid that is produced from tyrosine in the liver.  Through the action of the enzyme decarboxylase, it is converted in the brain to dopamine.  Dopamine is the neurotransmitter, the overactivity of which is hypothesized as the cause of the condition known as schizophrenia.

As mentioned earlier, the accumulation or activity of dopamine in the brain cannot be measured directly.  But one of the indirect measures of dopamine synthesis is the rate at which dopa is absorbed or taken up.  When 18 F-dopa (a radioactive analogue of dopa) is used, the uptake can be observed and measured on a positron emission tomography (PET) brain scan.  In these kinds of studies the rate of F-dopa uptake is normally expressed as a Ki value.


As mentioned earlier, there were three groups of participants.

a) Twenty-four “patients having prodromal symptoms of schizophrenia”. The authors describe these individuals as having an “at-risk mental state (ARMS)”. The concept is similar to the APA “diagnosis” of “attenuated psychosis syndrome” (DSM-5, p 122)

b) Seven “patients having schizophrenia.” All seven reportedly met the DSM-IV criteria for schizophrenia.

c) Twelve “matched healthy control subjects” recruited from the same geographic area as the clinic. No information is provided as to how these individuals were recruited or screened.

The results of the study are presented in Figure 2.

As can be seen, the diagram is divided into three vertical blocks: Control, ARMS, and Schizophrenia, reading from left to right.  The Ki values are shown on the vertical scale on the left.

The black horizontal rectangle (▬) indicates the mean Ki value for each group.  So the 12 controls had a mean of 0.0142; the ARMS group 0.0151; and the schizophrenia group 0.0157.  On the face of it, this looks like an impressive result.  The Ki values are steadily increasing across the three groups, strongly suggesting that dopamine synthesis capacity is increasing commensurately.

However, the individual scores in the three groups tell a somewhat different story.  Each diamond indicates the score for a healthy control subject; the triangles give the scores for each ARMS participant; and the round dots give the scores for the participants “diagnosed with schizophrenia.”  If we think of the healthy controls as having “normal” dopamine synthesis, then it is clear that Ki values between approximately 0.012 and 0.016 represent the normal range.  And it is also clear that the only study participants with values outside the normal range were three from the ARMS group and one from the schizophrenia group.  In other words, 87.5% (21 out of 24) of the ARMS participants, and 85.7% (6 out of 7) of the schizophrenia participants had Ki scores in the normal range.

The general point here is that mean values, although very useful and informative with some forms of data, can be quite misleading in other contexts.  On the basis of the findings presented in this study, I don’t think one could reasonably infer that there is “solid evidence for elevated presynaptic dopamine levels being a key abnormality in psychosis”, as Dr. Langford asserts.


Besides the marked overlapping of scores, there were other problems with the study. The first, and perhaps most obvious, is the problem of matched pairs.

In the paper’s abstract, the authors write:

“Twenty-four patients having prodromal symptoms of schizophrenia were compared with 7 patients having schizophrenia and with 12 matched healthy control subjects from the same community.”

This statement – particularly the word “matched” – conveys the impression that the “healthy control subjects” were similar to the members of the two focus groups in every respect except for those factors directly associated with a “diagnosis of schizophrenia” or “prodromal symptoms of schizophrenia”.  This is the essential assumption underlying all matched pairs research, and is a reasonably robust assumption for studies in physical science, engineering, materials testing, and even, to some extent, in general medicine.  In behavioral/psychological studies, however, the technique has serious limitations, because one would have to match on a dauntingly large number of variables to have even a remote chance that the two groups were sufficiently similar to enable one to draw even modest conclusions.

Here’s how it works in practice.  A researcher recruits individuals for his study.  The study might involve the administration of a treatment or, as in this case, observing something going on within the brain.  Let’s say that 20 people have been recruited.  The researcher then recruits 20 controls.  The controls are people who don’t have the feature under consideration (in this case, “schizophrenia symptoms”) but who do match the recruited participants (individual for individual) on a number of variables that are considered relevant.  So if the recruiter determines that age, gender, and education are the relevant factors, he would, for each participant, find a match:  a person of the same age, same gender, and same education.  So, if the experimental group responds to the treatment or yields different observations from those of the control group, one can have a measure of confidence in the validity of the results.

Most matched pairs studies provide a fairly detailed description of the matching process and the matching variables used.  This is not provided in Howes, Montgomery, Asselin, et al.  All we are told is that:

  • the controls were recruited from the same geographic area
  • the controls were “required to have no personal history of psychiatric illness”
  • and that the “…groups were well matched for variables that might putatively alter dopaminergic systems such as substance use and age…”

The point of all this is that, even if we allow that dopamine synthesis was higher in the striatal area of the brain for the ARMS and schizophrenic groups than for the controls, it is unsafe to conclude that excessive dopamine synthesis is a neurological abnormality inherent to individuals who attract the labels ARMS and schizophrenia.  It may be, for instance, that the dopamine difference is a reflection of some other factor entirely – something on which the controls and participants were not matched – e.g.  a history of abuse or victimization or the experience of failure. And we certainly have no grounds for believing that the dopamine excess causes the loose collections of vaguely defined thoughts, feelings, and behaviors that psychiatrists label “schizophrenia” and “attenuated psychosis syndrome”.

This last point is important because it touches on the unreliability of psychiatric “diagnoses”.  In studies of this sort, there is a tendency to accept the labels assigned to the different groups as 100% reliable.  So all members of the ARMS group are considered to “have” attenuated psychosis syndrome; all members of the schizophrenia group “have” schizophrenia; and all members of the control group are considered to be “healthy” – i.e. having  no psychiatric “illness”.  In reality, psychiatric evaluations are unreliable.  The kappa score for schizophrenia in the DSM-5 trials, for instance, was only 0.46.  So if we were to take the 43 people involved in the present study and present them to say ten other psychiatrists in a variety of settings, we will almost certainly get different groupings.  Some of the people in the focus groups will be considered “healthy” while conceivably some of those in the “healthy” group will be considered psychiatrically “ill”.

A further problem with the Howes, Montgomery, Asselin, et al study is the fact that one of the “patients” was taking quetiapine (100 mg/day) at the time of the study, and that others had apparently been taking neuroleptics in the past.  All that the authors tell us is that:

“All patients were not taking antipsychotic treatment for at least 8 weeks, except for 1 patient with ARMS who was taking quetiapine fumarate (100 mg/d[omitted for 24 hours before imaging])”

It is known that neuroleptic drugs affect the dopamine system, and it is a reasonable assumption that none of the control subjects had ever taken these products.  So we have another variable on which the groups were not matched.  It seems unlikely that the neuroleptic-induced dopamine changes in the brain would have dissipated within eight weeks.

Lest it be thought that I cherry-picked the Howes et al study, here’s the comparable Ki graph from another study cited by Drs. Howes and Kapur.  The study was conducted by Stephen McGowan et al (2004), Presynaptic Dopaminergic Dysfunction in Schizophrenia.

Here again, note that although the means differ in each analysis, there is a great deal of overlap when we look at individual scores.  For the entire striatum (A), 11 out of 15 (73.3%) “patients” have Ki values in the same range as the controls.  The corresponding Ki values for the ventral striatum (B) are 7 out of 11 (63.6%).  So here we have another group of people “with schizophrenia”, 60-70% of whom have normal Ki values.  In this study, incidentally, all the “patients” were taking neuroleptic drugs.

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

To return to Dr. Langford’s original assertion:

“An excellent summary by Kapur & Howes (referenced earlier in the report itself) and further imaging studies by Howes and others provide solid evidence for elevated presynaptic dopamine levels being a key abnormality in psychosis, and there is copious evidence that inhibiting the action of this excess dopamine using antipsychotics leads to clinical improvement in psychosis.”

It is noteworthy that Drs. Kapur and Howes themselves were a good deal less certain:

“Two different kinds of evidence could lead to a complete rejection of the hypothesis. PET studies directly implicating presynaptic dopamine dysfunction are a major foundation of this new version of the hypothesis. PET data require to be modeled to provide estimates of L-dopa uptake or synaptic dopamine levels—and the results are inferred rather than direct measurements. Thus, if it turns out that the body of evidence based on PET imaging is a confound or an artifact of modeling and technical approaches, this would be a serious blow for version III, though the data behind versions I and II would still stand strong. While possible, we think this to be highly unlikely. What is perhaps more likely is that a new drug is found that treats psychosis without a direct effect on the dopamine system. In other words, the dopamine abnormalities continue unimpeded, and psychosis improves despite them. A good example of such a new drug might be LY2140023, an mGlu 2/3 agonist. If this were to be an  effective antipsychotic and it could be shown that the new pathways do not show any interaction with the dopamine system, then the fundamental claim of version III, that it is the final common pathway, would be demolished. A similar situation would arise if a pathophysiological mechanism that does not impact on the dopamine system is found to be universal to schizophrenia. Much more likely is the possibility that the hypothesis will be revised but with a stronger version IV.” [Emphasis added]

So although Drs. Kapur and Howes express a general optimism for the hypothesis, they acknowledge that the theory could be demolished by future research.  And:

“The next decade will provide more information on the role of dopamine, particularly how genetic and environmental factors combine to influence the common pathway, and better drugs will be developed that directly influence presynaptic dopaminergic function—both logical successors to the idea of a final common pathway.”  [Emphasis added]

In the one Howes and Kapur reference that I reviewed (Howes, Montgomery, Asselin, et al 2009), the authors also express some cautionary notes:

“Results of recent clinical trials suggest that treatment with antipsychotic medication may reduce the severity of attenuated psychotic symptoms and the risk of schizophrenia in patients with ARMS.  Our finding of dopaminergic overactivity in the ARMS group indicates why drugs that act on the dopamine system may have these effects. We conclude that presynaptic striatal dopamine function may be a promising target for future drug development in the treatment of psychotic disorders.” [Emphasis added]


The acknowledgement statement at the back of the Howes and Kapur article states:

“Howes has received investigator-led charitable research funds or speaking engagements from AstraZeneca, Eli Lilly, and Janssen. Kapur has received grant support or has been a consultant/scientific advisor or had speaking engagements with AstraZeneca, Bristol Meyers Squibb, Eli Lilly, EMD—Darmstadt, Glaxo Smith Kline, Janssen (Johnson and Johnson), Neuromolecular Inc, Pfizer, Otsuka, Organon, Sanofi-Synthelabo, Servier, and Solvay Wyeth.”

The financial disclosure statement at the back of the Howes, Montgomery, Asselin, et al article states:

“Drs Howes, Montgomery, Murray, McGuire, and Grasby received investigator-led charitable research funds and honoraria from pharmaceutical companies manufacturing antipsychotic medication.”


The elevated dopamine synthesis hypothesis has been discussed by the British psychiatrist Joanna Moncrieff (The Myth of the Chemical Cure, 2009).  Here are three quotes:

“Another group of studies have measured the uptake of a radiolabelled dopamine precursor molecule, presumed to reflect the synthesis of dopamine in people with psychosis compared with healthy controls (Dao-Castellana et al. 1997; Elkashef et al.  2000; Hietala et al. 1995; Lindstrom et al.  1999; Reith et al.  1994).  Results of these are inconsistent.  Even the results of the ‘positive’ studies are incongruous with some finding increased uptake in the putamen but not the caudate nucleus (parts of the basal ganglia) (Hietala et al.  1995) and another finding increased uptake in the caudate but not the putamen (Reith et al.  1994).  One study found no effect (Dao-Castellana et al.  1997) and the largest study so far found the opposite finding of reduced uptake in the ventral striatal area of the brain (Elkashef et al.  2000).” (p 93) [Emphasis added]


“All recent studies were small, and although efforts were made to identify and include patients who had not previously taken neuroleptic drugs, known as ‘drug naïve’ patients, all but one of the studies also included patients who had taken these drugs in the past, often for long periods.  Therefore prior treatment with drugs known to affect the dopamine system may be, at least partially, responsible for the findings.” (p 93)


“However the biggest problem with all this research is the complete disregard for other possible explanations for increased dopamine activity.  Dopamine release is known to be associated with numerous activities and situations that may differ between patients and healthy controls and may account for the difference in dopamine activity independent of the presence of psychosis.  Motor activity and attention have been shown to increase dopamine activity and dopamine is involved in arousal (Berridge 2006).  People with acute psychosis are likely to be more aroused and agitated than healthy controls and this may account for increased dopamine activity.  None of the recent dopamine-psychosis studies have examined these possible confounders.” (p 93-94)


There is, in my experience, an unfortunate tendency among psychiatric practitioners to overstate their various chemical imbalance hypotheses, and to commensurately criticize, and even marginalize, those of us who offer alternative perspectives.  Dr. Langford’s assertion is a good example of this, and his rejection of the BPS’s statement as “bizarrely unfounded” borders on incivility.  There is nothing even remotely bizarre about the BPS statement, and, in fact, given the limitations of the studies cited, it is extremely well founded.

If psychiatry, at some time in the future, identifies a specific neurological abnormality, and demonstrates that this abnormality is present in all the people that they “diagnose with schizophrenia”, and in none of the people that are not so “diagnosed”, then they will indeed have established a key neurological abnormality associated with this condition.  If, by further research, they establish that the causal sequence is from neurological abnormality to the problematic thoughts, feelings, and behaviors of the individuals involved (as opposed, say, to the causality going the other way), then they will have uncovered something worth talking about.  And if, by still further research, they show that the abnormality is pathological rather than, say, a variation of normal functioning, then they will indeed have established that the condition known as schizophrenia can properly be regarded as a neuropathological condition.

But such evidence is not currently to hand.