Tag Archives: depression

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:  Still Blaming Everyone But Himself

On May 7, Allen Frances, MD, posted an article on the HuffPost site.  The piece was titled Antidepressants Work, But Only For Really Depressed People.

Superficially, the article presents itself as a call to limit the prescribing of the so-called antidepressant drugs to severe cases; but the piece can, I suggest, be more accurately characterized as Dr. Frances’s latest attempt to distance himself, and psychiatry in general, from the pill-peddling frenzy that has characterized the profession for the past thirty or forty years

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


“The biggest mistake in DSM III was introducing the very broad and heterogeneous category ‘Major Depressive Disorder’. This combined under one rubric what had previously been two separate and quite different presentations: 1) severe, melancholic, delusional, or incapacitating depressions, and 2) reactive to stress, mild, and often transient depressions. The result is that many people get the label Major Depressive Disorder, even though their presentation isn’t really ‘Major’, isn’t really ‘Depressive’, isn’t really ‘Disorder’. Mild sadness in reaction to stress and disappointment is lumped together with the most severe suffering known to man.”

At issue here is the old psychiatric distinction between endogenous depression and exogenous depression.  The later was conceptualized as a reaction to some external fact or circumstance, whereas the former was considered to have arisen from within the person – i.e. without any external loss or hurt.  The distinction was always problematic, in that it’s impossible to know, with certainty, that a person’s depression is not a response to some external loss, hurt, or circumstance, but the distinction was considered important within the psychiatric community generally.

In any event, the terms “exogenous” and “endogenous” went out of vogue, though the underlying concepts remained in place in DSM-III.  And, contrary to Dr. Frances’s assertion in the above quote, they remained in place as separate entities.  These were: “major depressive disorder”, and “adjustment disorder with depressed mood”.

In DSM-III, adjustment disorder is defined as “A reaction to an identifiable psychosocial stressor…”.  DSM-III made no provision for specifying severity of adjustment disorder (e.g. mild, moderate, severe), but in the text it states clearly that people may have “a more severe form of the disorder” or “only a mild form of the disorder”.  Major depressive disorder in DSM-III could be formally and explicitly coded as mild, moderate, and severe.

Now it’s no part of my agenda to defend any edition of the DSM, a document which in my view has all the scientific rigor and practical usefulness of a witch-hunter’s manual.  Rather, my purpose here is to point out that Dr. Frances’s assertion in the above quote is simply false.

Essentially what Dr. Frances is saying, or at least forcefully implying, is that since this great “error” in DSM-III, psychiatrists, misfortunate lambs that they are, have simply had no way to reflect in their “diagnostic assessments” that the individual’s depression “isn’t really ‘Major’, isn’t really ‘Depression’, isn’t really ‘Disorder’.”

And because of this truly arduous imposition, psychiatrists are constrained to lump “mild sadness in reaction to stress and disappointment” with “the most severe suffering known to man”.

It may well be that psychiatrists have been avoiding the use of “reaction to stress”, “mild” and “transient” qualifiers in their “diagnostic assessments”.  But this is emphatically not because such qualifiers were rendered impossible by DSM-III.  A much more likely explanation is that the use of these qualifiers militates against the notion, avidly promulgated by psychiatry for the past forty years, that depression, of whatever severity, is a chronic illness, (just like diabetes); a chemical imbalance in the brain, for which the “patient” must take so-called antidepressant drugs for an extended period, and possibly the rest of his/her life.  For all of this time, it has been an integral part of psychiatry’s informal, but avidly asserted, message that although depression might have been triggered by an external event, it is essentially an illness residing within the person’s neurochemistry.

But, even if we put all that aside; even if we acknowledge that Robert Spitzer and his DSM-III co-authors made a dreadful error, a critical question remains:  why did Dr. Frances himself and his DSM-IV co-authors, so uncritically follow suit?  And why has Dr. Frances not acknowledged his own perpetuation of this so-called error in the present paper?  It’s easy, and perhaps a little craven, to point fingers at the recently deceased Dr. Spitzer, when in fact, Dr. Frances himself followed precisely the same path.

And in fact, Dr. Spitzer was open enough to admit that he and his DSM-III co-workers had made a much more fundamental error.  Here’s a quote from an interview he gave to British film maker Adam Curtis.  The interview was screened by the BBC in 2007, and the 50 second excerpt can be viewed here, starting at minute 34:10.

Robert Spitzer, MD:

“What happened is that we made estimates of prevalence of mental disorders totally descriptively without considering that many of these conditions might be normal reactions which are not really disorders.  That’s the problem.  Because we were not looking at the context in which those conditions developed.”

Adam Curtis:

“So you have effectively medicalized much of ordinary human sadness, fear, ordinary experiences, you’ve medicalized them.”


“Uh, I think we have, to some extent.  How serious a problem it is is not known.  I don’t know if it’s twenty percent, thirty percent, I don’t know.  But that’s a considerable amount if it is twenty or thirty percent.”

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

Back to the Huffington Post piece.

“Drug companies jumped on the opportunity to peddle a pill for every problem and misleadingly described all depressions as a chemical imbalance requiring a chemical solution. Treatment studies that previously showed clear superiority of medicine over placebo for severe depression showed little or no superiority with patients whose depression was mild or questionable. And biological marker studies that showed promise in tagging severe depression came up empty with the watered down Major Depressive Disorder.”

There it is again.  Those mean old opportunistic drug companies!  How could one ever trust them?

But again, a major distortion of reality.  Drug companies can’t sell these products without FDA approval, and a physician’s prescription.  It was psychiatrists who created and promulgated the questionable research that elicited FDA approval and legitimized the wholesale use of these products.  Admittedly, these psychiatrists were handsomely paid by pharma, but they were not constrained.  Dr. Frances is surely familiar with this process.  In 1995, he and his two colleagues Drs. John Docherty and David Kahn, reportedly accepted $515,000 from Johnson & Johnson to write “Schizophrenia Practice Guidelines”, which blatantly promoted Risperdal (risperidone), a drug manufactured by Johnson & Johnson.  For a full and compelling account of this sordid tale, see Paula Caplan’s very thorough exposé here.

The notion that psychiatric research would clearly support the use of the drugs and would identify biological markers for depression, if only the “mild or questionable” depressions were excluded, is fanciful.  Depression has been extensively researched for decades, by psychiatrists, highly motivated by pharma largesse to find significant positive results.  These studies routinely report that “diagnoses” were confirmed by scrupulously careful evaluations using psychiatric interviews and validated screening tools.  So why would there by “questionable” cases in the studied samples?  In fact, in his Introduction to DSM-IV (1984), Dr. Frances explicitly acknowledged DSM-III’s contribution in this area.

“The third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) represented a major advance in the diagnosis of mental disorders and greatly facilitated empirical research.  The development of DSM-IV has benefited from the substantial increase in the research on diagnosis that was generated in part by DSM-III and DSM-III-R.” (p. xviii) [Boldface added]

An identical passage was included on page xxvi in DSM-IV-TR six years later (2000)

And furthermore, individuals whose depression is mild can be eliminated readily and legitimately from a study by limiting the scope to moderate and severe cases.


And what are we to make of Dr. Frances’s assertion that the drug companies “…misleadingly described all depressions as a chemical imbalance requiring a chemical solution”? In fact, it was psychiatry who promoted the chemical imbalance hoax.  Pharma certainly tagged along, with their blatantly false commercials, but psychiatry could have stopped this fraudulent inanity in its tracks at any time, by issuing a clear and definitive press release disavowing the hoax, and by filing a formal complaint of false advertising with the Federal Trade Commission.

But psychiatry took no such action.  Psychiatry blatantly, and without compunction, foisted this falsehood on their “patients”, on the public, and on other practitioners – knowing it to be false – for the purpose of promoting their own guild interests, and selling more drugs.  It is simply beyond comprehension that Dr. Frances continues to try to slough off the responsibility for this hoax, this gross violation of the public trust, onto his erstwhile pharma benefactors.

If Dr. Frances has any residual doubts as to psychiatry’s role in the dissemination of this falsehood, he might usefully take a look at Terry Lynch’s book Depression Delusion or my post Psychiatry DID Promote the Chemical Imbalance Theory

Or … he might want to revisit something he himself wrote in 1998.  Here’s a quote from Am I Okay? by Allen Frances, MD, and Michael B First, MD:

“Depression is really no different than hypertension.  Medicines that treat high blood pressure are taken to reestablish the body’s ability to maintain a normal blood pressure.  Antidepressants work in the same way—restoring brain neurochemistry to its original natural state.  In contrast to drugs like heroin and cocaine, which make virtually everyone feel euphoric, an antidepressant does nothing for a person without depression except produce unpleasant side effects.  There is no street market for antidepressants and they are not addictive.  Finally, in the same way that it would be ludicrous to think that someone can simply will their elevated blood pressure down to normal, true grit is not by itself sufficient to cure clinical depression.” (p 49-50)  [Emphasis added]

Incidentally, Dr. Frances’s promotion of the now defunct chemical imbalance theory of depression in the above quote is particularly interesting in the light of the statement made by the very eminent psychiatrist Ronald Pies, MD in his April 2014 article Nuances, Narratives, and the Chemical Imbalance Debate:

“To the extent the ‘chemical imbalance’ notion took hold in our popular culture, it was due mainly to distorted or oversimplified versions of the catecholamine hypothesis. These were often depicted in drug company ads; pop psychology magazines; and, in recent years, on misinformed Websites and blogs. In short, the ‘chemical imbalance theory’ was never a real theory, nor was it widely propounded by responsible practitioners in the field of psychiatry.”

Dr. Pies, meet Dr. Frances.

With regards to Dr. Frances’s assertion that there is no street market for antidepressants, here is a letter in the February 2007 issue of the American Journal of Psychiatry.  The letter is from Greg Tarasoff, MD, a psychiatrist, and Kathryn Osti, and is titled Black-Market Value of Antipsychotics, Antidepressants, and Hypnotics in Las Vegas, Nevada. The letter reports that, at that time, antidepressants were selling on the street for $3-$5 per dose.

Also, here’s a 2013 article from globalnews.ca, Toronto, which describes an active street market in Wellbutrin.  The article was written by Jennifer Tryon and Nick Logan, and it reports that Wellbutrin is referred to as “the poor man’s cocaine”.

I realize, of course, that Am I Okay was written before these articles, but here are two studies that predate the book:

Abuse of Amitriptyline by Cohen, Hanbury, and Stimmel: JAMA, Sept 1978:

“A survey of 346 persons enrolled in a methadone maintenance program showed that 86 (25%) had admitted taking amitriptyline with the purpose of achieving euphoria.”

And Identification of misused drugs in the clinical laboratory. I. Tricyclics, by Vasiliades, J; Clinical Biochemistry, February 1980:

“A systematic approach evaluating the abuse of tricyclic drugs in the hospital emergency room from the laboratory point of view is presented…Increasing misuse of tricyclic antidepressants requires that the clinical laboratory have a systematic approach to identify and confirm the presence of these drugs in emergency room patients.” [Emphasis added]

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


Back to Am I Okay?  Here’s a quote in which Drs. Frances and First promoted the drugs as “very effective” in the treatment of “major depressive disorder”:

“For those suffering from Major Depressive Disorder, antidepressant medications are very effective—the overall odds that an antidepressant treatment will work eventually are probably at least 90 percent.  But you have to be patient and forbearing along the way.  It usually takes at least several weeks for the medication to begin working, and a couple of months before it has reached its maximum effect.  It might also take time and effort to find the most effective medication for you and to determine its proper dose.  Some people must endure several trials of different antidepressants until they find the one that is a winner for them.  To give you some perspective, two thirds of depressed patients will have a good response to the first medicine that is tried. For those who do not respond initially, the odds of a second antidepressant working are about fifty-fifty—this gets us to about 80 percent total response rate.  If you have still not yet responded after two tries, a third or fourth or even a fifth try may be necessary to find the medicine or combination of medicines that will eventually work.  The good news is that there are close to thirty available antidepressants on the market and new ones are being developed all the time.  Hopefully sooner, but almost certainly eventually, one of these or some combination will work for you.

The use of antidepressant medication has risen dramatically over the past several years, but many people who might benefit have misconceptions that make them reluctant to give one a try.  One common concern is that the changes resulting from antidepressant use are artificial and, by implication, somehow illegitimate.  Others worry that they will become physically dependent on antidepressants in the same way that a heroin addict cannot function without his daily fix.  Yet others feel that having to rely on antidepressant medications to maintain one’s mood (and productivity) represents a weakness in moral fiber—that you should be able to get rid of the depression by sheer will power alone.” (p 49)

There are several noteworthy points in this quote.

Firstly, Dr. Frances does not limit his assertions to cases of “severe, melancholic, delusional, or incapacitating depressions“, even though such options were available within the psychiatric “diagnostic” system.  The phrase “…those suffering from Major Depressive Disorder” clearly embraces mild, moderate, and severe unless otherwise delineated.  In fairness to Dr. Frances, he does acknowledge elsewhere in the text that the drugs are not always necessary, but his assertions in this regard are generally less compelling, e.g., “antidepressant medications are probably overused.” (p 50) [Emphasis added]

Secondly, the tone of the quote with regards to taking the drugs is upbeat and optimistic.  The drugs “…are very effective”; “the odds of successful treatment…are probably at least 90 percent”; “…there are close to thirty available antidepressants on the market…”; “…one of these or some combination will work for you.”

Thirdly, the authors acknowledge that antidepressant use has risen “dramatically”, but then go on to encourage further use.

Fourthly, there are clear efforts on the part of the authors to undermine people’s resistance to drug-taking. The authors dismiss concerns that the effects of the drugs are “artificial” and that the drugs might be addictive.  Bearing in mind that the book was written for general audiences (A Layman’s Guide to the Psychiatrist’s Bible), the assertion that antidepressants restore “…neurochemistry to its original natural state”, with its almost Edenic connotations, is nothing short of outrageous.

And incidentally, here’s another quote from the same chapter:

“ECT is a terrifically effective treatment  that is also relatively safe considering the great benefits that can often be gained.  ECT is especially useful for psychotic mood disorders, people who need a really fast response, medication nonresponders, and for those who cannot tolerate antidepressant medication.  Electroconvulsive therapy has a higher response rate (80 to 90 percent versus the 65 to 70 percent achieved by medication combinations) and also works more rapidly.  However, it has the disadvantage of providing fewer clues as to what type of medication is likely to work to prevent recurrences in the maintenance phase.  Due to misguided fears, ECT has been most typically considered a treatment of last resort when nothing else works.  It probably deserves to be used earlier and more often.” (p 51-52)

Note that the success rate of antidepressants which on page 49 was given as “at least 90 percent”, is now, two pages later, given as “65 to 70 percent”.

Note also that Dr. Frances is advocating an expansion of the use of high voltage electric shocks to the brain as a “treatment” for depression, and makes no mention of the permanent memory damage that this “treatment” entails.

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

Back to the HuffPost article:

“Critics of medication jumped on this to argue misleadingly that depression is a myth and/or that medication treatment for depression doesn’t work.”

I don’t know of anyone on this side of the debate who argues that “depression is a myth”.  I myself argue – as do a great many others – that depression is not an illness.  But depression is real, and I don’t believe that I’ve ever heard anyone suggest otherwise.  My own position is that depression is the natural human reaction to loss or to ongoing hardship/drudgery, and that severe depression is the normal reaction to a major loss or to ongoing hardship/drudgery that is particularly arduous.  It is not something that needs to be “treated”; rather, it can be alleviated, either by supporting individuals through their loss, or actively helping them identify and extricate themselves from the depressing circumstances.  What the pills do, in some cases, is provide an altered mental state, which some people find preferable to the depression.  But the pills produce no lasting benefits, and usually do a great deal more harm than good.  The issue here is not whether people should or shouldn’t take these pills.  That’s each person’s individual choice.  The issue is psychiatry pushing these dangerous serotonin-disruptive chemicals on people, under the pretense that they have an illness, for which the pills are an effective and safe treatment.

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

At this point in the article, Dr. Frances introduces Mark Kramer, MD, PhD.  Dr. Kramer restates and elaborates on some of the points made by Dr. Frances, who in turn closes the article with some concluding remarks, including:

“The next point seems too obvious to be stated, but nonetheless desperately needs stating. Only people who are clearly clinically depressed and clearly need antidepressants should be included in research studies and should be taking antidepressants in everyday clinical practice. Depression has been too carelessly diagnosed- encouraged by the loose DSM definition, by Pharma’s desire to push product; by rushed doctors; and by people’s hope for a quick fix for life’s problems.”

It should be noted that the term “clinically depressed”, despite its widespread usage, has no formal meaning in psychiatry.  In practice, it is used to mean having a “diagnosis” of major depressive disorder or dysthymia, but because of the medical connotations of the word “clinical”, it is also used to convey and promote the notion that depression is an illness.  So Dr. Frances is telling us that only people who clearly meet the criteria for major depressive disorder or dysthymia, and who clearly need antidepressants, should be taking antidepressants.  But this is nothing more than an empty platitude.  What’s the alternative?  Take antidepressants even though you don’t really need them?  Who is suggesting that? And anyway, wasn’t the whole point of the DSM to provide rigorous definitions of the various “mental disorders”?  Hasn’t this been the standard psychiatry patter since DSM-III?  In fact, here’s the opening paragraph from the Introduction to Dr. Frances’s own DSM-IV:

“This is the fourth edition of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, or DSM-IV.  The utility and credibility of DSM-IV require that it focus on its clinical, research, and educational purposes and be supported by an extensive empirical foundation.  Our highest priority has been to provide a helpful guide to clinical practice.  We hoped to make DSM-IV practical and useful for clinicians by striving for brevity of criteria sets, clarity of language, and explicit statements of the constructs embodied in the diagnostic criteria.  An additional goal was to facilitate research and improve communication among clinicians and researchers.  We were also mindful of the use of DSM-IV for improving the collection of clinical information and as an education tool for teaching psychopathology.” (p xv)

and later, concerning DSM-III:

“DSM-III introduced a number of important methodological innovations, including explicit diagnostic criteria, a multiaxial system, and a descriptive approach that attempted to be neutral with respect to theories of etiology.” (p xvii-xviii)

So if the problem is “loose DSM definitions”, Dr. Frances needs to direct at least some of the responsibility for the present state of affairs in his own direction; firstly for drafting a document that slavishly followed the errors he now ascribes to DSM-III, and secondly for  falsely hyping DSM-IV in that edition’s Introduction.

In should also be noted, that the “diagnostic” definitions in all editions of the DSM are notoriously vague and “loose”.  But in addition, Dr. Frances’s own DSM-IV added an entire layer of looseness:

“The specific diagnostic criteria included in DSM-IV are meant to serve as guidelines to be informed by clinical judgment and are not meant to be used in a cookbook fashion.  For example, the exercise of clinical judgment may justify giving a certain diagnosis to an individual even though the clinical presentation falls just short of meeting the full criteria for the diagnosis as long as the symptoms that are present are persistent and severe.” (p xxiii) [Emphasis added]

How short is “just short”?  What duration would be considered persistent?  In the case of “major depressive disorder”, we know that “persistent” means two weeks!

Dr. Frances tells us that depression (by which he clearly means the mythical illness) has been too carelessly diagnosed by

– pharma’s desire to push product;
– rushed doctors (note, not specifically psychiatrists); and
– people’s hope for a quick fix for life’s problems

In short:  everyone is to blame for the drug-pushing except psychiatry; that dauntless and noble pillar of compassionate rectitude, standing valiantly alone against the surging tide of venality, corruption, disease-mongering, slovenliness, and disempowerment that characterizes all the other players in this epic tragedy.

The notion that the loose definitions, the inexorable expansion of the “diagnostic” net, and the broadening of “indications” for the drugs were errors, is simply not credible.  If these were errors, then psychiatrists must surely be a most inept group of people.  Rather, these developments were, and still are, an integral part of psychiatry’s plan to expand its scope and to strengthen its hegemony.  And this plan, in the implementation of which Dr. Frances played a leading part, is still in place.  Psychiatry, with the help of their pharma allies, is actively promoting early screening for various “diagnoses”.  Active steps are being taken to have mental health services embedded in every school and in every GP’s office.  Children as young as three years old are being given major tranquilizers to “treat” temper tantrums, and vulnerable individuals in nursing homes, foster care, and group homes are being drugged at unprecedented levels.

If Dr. Frances genuinely wants to distance himself from this institutional degeneracy, he must first acknowledge the role that he himself played in its creation.


Important as all these issues are, there is a fundamental, over-riding issue that is much more critical.

The assertion that the so-called antidepressants are being over-prescribed implies that there is a correct and appropriate level of prescribing towards which reformative efforts should be directed.

And this premise is false, for three reasons.  Firstly, because depression, regardless of its severity or persistence, is not an illness which needs to be treated with medication.  Secondly, because the drugs, despite the psychiatric-pharma hype, are not particularly effective in ameliorating depression.  And, thirdly, because these serotonin-disruptive drugs have a wide range of adverse effects, the seriousness of which has been routinely downplayed by pharma and by psychiatry.

The widespread and increasing use of the so-called antidepressant drugs is certainly a matter for concern, as is the assignment of depression “diagnoses” to more and more people.  But these problems stem directly and inevitably from the fact that psychiatry invented these spurious illnesses and generated the bogus research to legitimize the use of the pills as safe and effective “treatments”.  Given the inherent vagueness of the criteria and the absence of an identified and confirmable biological pathology, it was inevitable and predictable that “diagnosing” and pill-pushing would increase. To put the matter briefly, there is no way to determine who has the illness called depression and who doesn’t, because no such illness exists.  Psychiatry invented this entity, concocted an inane checklist of “symptoms” to create the appearance of medical legitimacy, peddled the pills with abandon, and reaped the profits.

Allen Frances’s bemoaning the “over-prescribing” at this late stage in the game is not only hypocritical.  It also serves to distract his readers from the real issue:  that psychiatry is, at its very core, an enormous and destructive hoax, and cannot be saved from its own self-serving excesses by these kinds of platitudinous calls to clean house.

The Germanwings Crash:  Flying Under the Influence

On March 24, 2015, a twenty-seven-year-old German pilot named Andreas Lubitz flew an Airbus A 320 into a French mountainside, killing himself and the 149 other people on board.  Mr. Lubitz was co-piloting the flight, and he caused the aircraft to crash by locking the pilot out of the flight deck and setting the autopilot to descend to 100 feet.

During the descent, he was contacted by civilian and military traffic controllers, and by the crew of another aircraft, but he made no response.  He also ignored repeated and increasingly urgent requests from the captain to be readmitted to the flight deck.

In an earlier flight on the same day, Mr. Lubitz had set the autopilot to descend from 35,000 feet to 100 feet, and returned it to the original setting after three seconds.  Investigators suggested that this earlier maneuver may have been a rehearsal for the subsequent murder/suicide.


The crash was investigated by the French Bureau d’Enquêtes et d’Analyses (BEA), who issued their final report on March 13, 2016.  Here are some of the findings from this report.

Mr. Lubitz had become depressed in August 2008 and had received psychiatric treatment, including psychiatric drugs, between November 2008 and July 2009.

Mr. Lubitz had been rated “above standard” on professionalism and skill by his instructors and examiners.

Mr. Lubitz’s private physicians refused to be interviewed by the BEA.

On February 24, 2015, four weeks before the murder/suicide, Mr. Lubitz received his first prescription of mirtazapine from his psychiatrist.  Mirtazapine, which is marketed in the US as Remeron, is an antidepressant with serotonergic activity.  Adverse effects include suicide risk, apathy, and aggression (RxList).  In the US, mirtazapine carries a suicide risk black box warning.

On March 16, 2015, eight days before the murder/suicide, Mr. Lubitz received further prescriptions of Escitalopram, Dominal, and Zolpidem from his psychiatrist.  Escitalopram, which is marketed in the US as Lexapro, is an SSRI antidepressant, and also carries a suicide black box warning.  Dominal (prothipendyl) is described as having a weak anti-psychotic potency (Wikipedia, translation from German), and is used to reduce restlessness and agitation.  Zolpidem (marketed as Ambien) is a sleeping pill.

In an email sent to his psychiatrist in March 2015, Mr. Lubitz stated that he had taken additional drugs:  Mirtazapine (15mg) and Lorazepam (1 mg).

Toxicological examination of the co-pilot’s human tissue found at the crash site detected the presence of citalopram and mirtazapine (both anti-depressants), and zopiclone (a sleeping pill).


Since the publication of the BEA Final Report, concerns have been expressed by various individuals and groups, including bereaved relatives of the victims.  In general, these concerns have focused on the following issues:

  • That Lufthansa (the parent airline) should have done more to protect their customers.
  • That because of medical confidentiality, Mr. Lubitz was able to hide his depression and his use of antidepressant drugs from his employer.
  • That several of the doctors involved in Mr. Lubitz’s care refused to provide information to the BEA investigators.
  • That Mr. Lubitz had managed to keep his pilot’s license, despite his history with depression and psychiatric drugs.

But there has been relatively little attention focused on what is, at least in my view, the most glaring and pertinent aspect of the matter:

That Mr. Lubitz was flying a commercial aircraft under the influence of powerful psychiatric drugs that have long been associated with murder/suicides.


On September 14, 1989, a few weeks after he had started taking Prozac (the first SSRI), Joseph Wesbecker, of Louisville, Kentucky, went on a rampage at his place of employment, killing eight and wounding twelve others, before taking his own life.  Eli Lilly, the makers of Prozac, settled the subsequent litigation for an undisclosed sum that was said to be “mind boggling” (Joseph Glenmullen, Prozac Backlash, 2000, p. 176).  In the interim years, there have been numerous similar incidents.

It is now 36 years since Drs. Teicher, Glod, and Cole wrote:

“Six depressed patients free of recent serious suicidal ideation developed intense, violent suicidal preoccupation after 2-7 weeks of fluoxetine treatment. This state persisted for as little as 3 days to as long as 3 months after discontinuation of fluoxetine. None of these patients had ever experienced a similar state during treatment with any other psychotropic drug.” American Journal of Psychiatry, 1990. [Fluoxetine, marketed as Prozac, is an SSRI]

Over the next two years, similar reports appeared in the New England Journal of Medicine, Journal of the American Academy of Child and Adolescent Psychiatry (here) and (here), Journal of Family Practice, American Journal of Psychiatry (here) and (here), Archives of General Psychiatry, Human Psychopharmacology, and the Lancet.

And similar tragic incidents have occurred with more recent drugs that tamper with the brain’s serotonin systems.

Nevertheless, psychiatry, to its eternal shame, has made no attempt to study definitively the role that psychiatric drugs play in these matters.  Instead, there has been spin:  more “treatment” is needed for “mental illness”; these drugs are safe when “properly prescribed”; the benefits outweigh the risks; etc…

It was even stated, by Connecticut Assistant Attorney General, Patrick B. Kwanashie, in the wake of the Sandy Hook murders/suicide that it would not be wise to divulge the drugs found in the shooter’s post-mortem examination, for fear that it would “… cause a lot of people to stop taking their medications.”

Even the horrific events of March 24, 2015, in the French Alps have been insufficient to jar psychiatry from its sordidly self-serving, guild-defensive silence into something resembling common decency.  It took ten minutes for the Airbus to descend from 38,000 feet to its crash site on a French mountain; ten minutes of indescribable terror for 149 innocent men, women, and children.  It is time – indeed it is long past time – for psychiatry to acknowledge the role that these pills are playing in these tragedies, to conduct a definitive study of this matter, and to publicize the problem honestly and prominently.

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

On February 26, 2016, David Jolly, a member of the US House from Florida’s 13th District, introduced a bill directing the Department of Veterans’ Affairs to complete a publicly available review of the deaths of all veterans who died by suicide during the preceding five years.  The review would include a list of all medications prescribed to, and found in the system of, such veterans at the time of their deaths.

On March 7, the bill was sent to the Subcommittee on Health.  It will be interesting to watch its progress or lack thereof.  It will be interesting to see if politicians have more courage to buck their pharma paymasters than psychiatrists.  They certainly couldn’t have less.

Gender Wage Gap and Depression/Anxiety

In their January 2016 issue, the journal Social Science and Medicine published Unequal depression for equal work? How the wage gap explains gendered disparities in mood disorders, by Jonathan Platt, MPH, Seth Prins, PhD candidate, Lisa Bates, PhD, and Katherine Keyes, PhD, MPH.  All the authors work at Columbia’s Department of Public Health.

Here’s the abstract:

“Mood disorders, such as depression and anxiety, are more prevalent among women than men. This disparity may be partially due to the effects of structural gender discrimination in the work force, which acts to perpetuate gender differences in opportunities and resources and may manifest as the gender wage gap. We sought to quantify and operationalize the wage gap in order to explain the gender disparity in depression and anxiety disorders, using data from a 2001-2002 US nationally representative survey of 22,581 working adults ages 30-65. Using established Oaxaca-Blinder decomposition methods to account for gender differences in individual-level productivity, our models reduced the wage gap in our sample by 13.5%, from 54% of men’s pay to 67.5% of men’s pay. We created a propensity-score matched sample of productivity indicators to test if the direction of the wage gap moderated the effects of gender on depression or anxiety. Where female income was less than the matched male counterpart, odds of both disorders were significantly higher among women versus men (major depressive disorder OR: 2.43, 95% CI: 1.95-3.04; generalized anxiety disorder OR: 4.11, 95% CI: 2.80-6.02). Where female income was greater than the matched male, the higher odds ratios for women for both disorders were significantly attenuated (Major Depressive Disorder OR: 1.20; 95% CI: 0.96-1.52) (Generalized Anxiety Disorder OR: 1.5; 95% CI: 1.04-2.29). The test for effect modification by sex and wage gap direction was statistically significant for both disorders. Structural forms of discrimination may explain mental health disparities at the population level. Beyond prohibiting overt gender discrimination, policies must be created to address embedded inequalities in procedures surrounding labor markets and compensation in the workplace.”

In other words, when women were receiving less pay than men for the same work, they were about two and a half times more likely to “have major depressive disorder”, and about four times more likely to “have generalized anxiety disorder” than their male counterparts.  But when women were earning more than men, the odds were 1.2 and 1.5 respectively.

The use of psychiatric terminology (“major depressive disorder” and “generalized anxiety disorder”) constitutes something of a barrier to communication here, but the general message is clear:  people (in this case women) who are routinely treated unfairly and discriminately are more likely to be depressed and anxious, than those not so treated.

This is hardly surprising.  Depression and anxiety are not illnesses.  They are adaptive mechanisms – messages from our bodies alerting us to the need to make changes.  So, for instance, a person living in a high crime neighborhood might experience depression and anxiety.  These feelings are not symptoms of an illness.  Rather, they are the normal and appropriate emotional concomitants to the knowledge that one’s living arrangements are not safe, wholesome, or comforting.

The feelings of depression and anxiety are, in effect, a “nudge” from the body to move to safer surroundings, analogous to the urges that animals feel to move to higher ground in time of flooding, or to move to warmer latitudes as winter approaches.

But in a great many cases, the individual is unable to move, either because of family ties, lack of means, or other reasons.  So the urge to move lies unrequited, where it grows stronger, and saps the person’s energy and will.  The feelings of hopelessness, anhedonia, worthlessness, and guilt, codified in the DSM as “symptoms” of the “illness, major depressive disorder” are in fact the eminently appropriate response to being trapped in an untenable but inescapable situation.

And in this regard, gender wage discrimination is an extremely fast-holding trap.  Even if the victim can manage to find another job, there is every likelihood that the wage discrimination will be as strong as it was in her previous position.

Platt et al found that women in a large US nationally representative sample were earning only 54% of men’s pay.  This figure, when adjusted for productivity, was increased to 67.5%.  But even by the latter reckoning, this is an enormous difference.  For every man earning $30,000 per year, his matched female counterpart was earning about $20,000.  Over a forty-year working career, this amounts to a $400,000 disparity.

Quoting again from Platt et al:

“In sum, there are robust and long-standing gender disparities in depression and anxiety disorders, in addition to persistent gender disparities in wages. Although the latter are somewhat reflective of differential individual-level attainment of characteristics conducive to productivity, a large proportion of this gap remains after accounting for these factors and is likely the result of discriminatory processes operating at structural, institutional, and individual levels. This ‘unexplained’ portion appears to be increasing.”

So what we’re seeing here is one more piece of evidence that depression is not an illness to which women just happen to be “prone”.  Rather, it is an entirely appropriate and realistic response to an intolerable situation.  And when the situation can’t be escaped, the depression becomes, understandably, an abiding and persistent sense of joylessness and unfulfillment.  And when this kind of discrimination is combined with the fact that many employed women come home to another five or six hours of housework and childcare, the joyless treadmill factor increases enormously.

Psychiatry then enters the picture, proclaiming with its customary unsupported assurance, that episodes of depression and anxiety that cross arbitrary and vaguely-defined thresholds of severity, frequency, and duration, regardless of their source, are illnesses – just like diabetes.  These illnesses are caused by deficits of neurochemicals for which, by great good fortune, psychiatry has “very effective” remedies in the form of pills and high voltage electric shocks to the brain.

Psychiatry also has an “explanation” for the gender gap disparity in depression.  On the NIMH website you will find a page called Depression in Women.  There’s a section headed “What causes depression in women?”  Here’s the section quoted in full:

“Several factors may contribute to depression in women.

Genes—women with a family history of depression may be more likely to develop it than those whose families do not have the illness.

Brain chemistry and hormones—people with depression have different brain chemistry than those of people without the illness. Also, the hormones that control emotions and mood can affect brain chemistry.

During certain times of a woman’s life, her hormones may be changing, which may affect her brain chemistry. For example, after having a baby (postpartum period), hormones and physical changes may be overwhelming. Some women experience postpartum depression, a serious form of depression that needs treatment. Other times of hormonal change, such as transition into menopause, may increase a woman’s risk for depression.

Stress—loss of a loved one, a difficult relationship, or any stressful situation may trigger depression in some women.”

So there it is:  genes, brain chemicals, hormones, and stress.  Stress, of course, is a valid consideration here, but note how the NIMH has worded it:  “Stress…may trigger depression…”  Trigger is a firearms analogy and denotes a relatively minor event that initiates a major event in a system that is already prepared and primed.  So, the loss of a loved one – to use the NIMH’s own example – doesn’t cause feelings of despondency and depression; rather, it triggers these feelings in “some women”, presumably those already primed with “different brain chemistry” and depression-prone genes.

The Platt et al study is thorough and meticulous and was picked up by several mainstream media, including the Wall Street Journal, the New York Times, and the Guardian.  But I have not been able to find a single mention of it on any psychiatry-promoting site.  This is the same psychiatry that consistently asserts its commitment to a biopsychosocial perspective.

Book Review:  Depression Delusion, by Terry Lynch, MD, MA

In this truly remarkable, and meticulously researched, volume, Dr. Lynch annihilates psychiatry’s cherished chemical imbalance theory of depression.  Every facet of this theory, which the author correctly calls a delusion, is critically analyzed and found wanting.  Example after example is provided of psychiatrists promoting this fiction, the factual and logical errors of which are clearly exposed in Dr. Lynch’s lucid, seamless, and highly readable prose.

The book runs to 343 pages, and is laden with factual details, case studies, alternative perspectives, and hard-hitting commentary.  Dr. Lynch does not sit on the sidelines, nor does he seek any kind of collegial compromise with the chemical imbalance theory, which he unambiguously denounces as a groundless and destructive falsehood.  Here are some quotes that I think will convey something of the content, style, and cogency of this vitally important work.

“The world is engulfed in a mass delusion regarding depression.  The widespread belief that brain chemical imbalances are present in depression has no scientific basis.  In fact, this is a fixed belief that meets all the criteria of a mass delusion.  If you are one of the millions of people who believe that biochemical brain imbalances are known to occur in depression, then you too have become seriously misinformed.” (p 1)

“Despite the obvious complexity of the brain, some psychiatrists and GPs profess an understanding of this organ that is highly inconsistent with current scientific knowledge.  Their comments smack of a level of arrogance that in my opinion is downright dangerous.” (p 65)

“The brain chemical imbalance delusion has dominated medical, psychological and public thinking about depression for the past fifty years.  Parties with a vested interest see nothing wrong with this.  Nor do the vast majority of the general public, for whom the depression brain chemical imbalance idea feels as familiar and logical as raised blood sugar in diabetes.  There are two main reasons why psychiatrists and GPs have embraced the biochemical imbalance delusion with such enthusiasm.  This notion portrays doctors and their drug treatment in a positive light, as real doctors treating biological abnormalities consistent with the treatment of diseases generally in medicine.  Secondly, having observed for thirty years how my medical colleagues in psychiatry and general practice work, I do not believe they know any other way of understanding or responding to depression other than as an assumed biological abnormality.  I remain unconvinced that there is sufficient breadth of vision within mainstream psychiatry or medicine to see or to move beyond the rigidly held belief that depression is primarily a biological disorder.  Yet, the majority of the experiences categorized as depression are primarily emotional and psychological or have a significant emotional input.” (p 77)

“It is misleading to state that the brain chemistry of depression is not fully understood, when in truth it is really not understood at all.  It is also misleading to state that ‘research suggests’ that ‘depression is caused by an imbalance’ of brain chemicals.  It is drug companies, doctors and researchers who suggest this, not the research itself. As outlined in detail earlier the research itself does not suggest this at all and indeed contradicts this notion.” (p 149)

“In twenty years as a medical doctor, I have never, ever heard of a patient anywhere having their serotonin levels checked.”(p 153)

“Low serotonin cannot ever be identified since brain serotonin cannot be measured and we do not know what serotonin levels should or should not be.” (p 165)

“Providing societies with an apparently trustworthy rationale for avoiding the reality of human distress has resulted in increasingly costly mental health services within which recovery is a far rarer outcome than it should be.  Since the core issues are repeatedly side-stepped, they are not addressed or recognized within these mental health systems.  It is not surprising that the costs of such systems keep increasing with little hard evidence that these systems are providing value for money in terms of recovery.” (p 237)

“The most beneficial position for psychiatry is therefore the one that currently pertains.  By nailing its colours to the biological mast, psychiatry has successfully set itself apart from talk therapies.  As long as no biological abnormalities are reliably identified, there is no threat that their bread and butter will be removed from them to other medical specialties.  Maintaining the myth that biological solutions are just around the corner satisfies the public and maintains psychiatry’s position quite satisfactorily from psychiatry’s perspective, albeit between a rock and a hard place.  This position has no solid scientific foundation, but as long as the public do not realize this and psychiatry does not attempt to encroach on the territory of other medical specialties such as neurology, psychiatry’s position is secure.”  (p 277)

“When basic principles of correct reasoning and science are applied to the brain chemical imbalance idea, the flaws and inconsistencies of this belief become obvious.  When the depression brain chemical imbalance idea is rigorously examined, we find that like the emperor, it has no clothes.  These flaws and inconsistencies were known prior to Prozac coming on stream in 1988.  They were dismissed because they risked ruining a great story, from which many groups could profit enormously.” (p 342)

For those who wish to pursue topics further, there is a reference list at the end of each chapter.  There is also a comprehensive index and table of contents which make it easy to find specific sub-topics.

Pharma-psychiatry’s chemical imbalance theory of depression is one of the biggest and most destructive hoaxes in human history.  Dr. Lynch’s Depression Delusion might well be the work that finally lays this hoax to rest, and exposes the self-serving deceptiveness that has become a routine part of psychiatry’s endeavors.

Please read this book, keep it close to hand for reference, and encourage others to read it also.  Ask your library to buy a copy.  The spurious chemical imbalance theory is now so widely accepted that it will take enormous efforts to dislodge it.  In any debate on this matter, Dr. Lynch’s book will, quite literally, put the facts at your fingertips.

You Are Stronger Than What You Think

This post was submitted by a reader.






No, I’ve never used the services of psychologists, never took a
But I have felt under sudden Depression and Anxiety, like any of you.
Self awareness is necessary. To know when you are not acting
If we keep hoping for something to happen in an unrealistic way, on
denial, and at the end of the journey we cannot achieve that goal,
How do I beat it?
Redirecting my mind to most realistic goals.
Recharging my mind with optimism, remembering the beautiful things we
have achieved already.
Admiring Nature, the smile of a kid: LOVING.
Exercises help. Art too.
The most important thing?
Think you have come to this world with a purpose.
Think you can help others.
Feel like a champion who can accomplish everything.
And stay away from medication:
The cure is inside you, in your mind, in your soul…
Be strong!


A Reader

Depression:  A Different Perspective

I have recently come across an interesting paper:  How to Understand and then Escape from Depression.  It’s written by Saul Youssef, a professor of physics at Boston University.

The central theme of the paper is that persistent or chronic depression is caused by “…an unconscious withdrawal of participation in a person’s own internal decision making processes.”

Here are some quotes:

“I have been depressed for most of my life, and, at various times, I have tried most of the recommended treatments for depression. I have tried Saint John’s Wort, exercise, Yoga, talk therapy, SSRIs, thyroid supplements and Cognitive Behavioral Therapy. In my case, I would say that thyroid supplements, exercise and Yoga helped the most and all of them helped at least a little bit.  Unfortunately, none of these treatments helped dramatically. Then, however, in late 2013 and early 2014, I finally figured it out. I came to understand what was happening in my own head and why it was causing my own depression and I was able to figure out a way to escape. I don’t mean that I am now successfully managing my depression. I mean it’s gone. I am writing up what I think is going on and what I did to escape because I don’t think that my case is unusual. I think that exactly the same thing will work for many people.”

“A depressed person continues to live, but they do not continue to decide.”

“A depressed person is mainly on autopilot without realizing that they are mainly on autopilot. A depressed person will do what they always do, say what they always say, feel what they always feel and think what they always think.”

“If a depressed person actually has to do something, and they don’t decide anything, how do they do it? The answer is that they wait until an unconscious process forces them to do it. If a depressed person has to do their taxes, for instance, they will not decide at some moment to do their taxes. Instead, they will wait until the fear of the consequences of not doing their taxes forces them into doing their taxes. Depressed people will procrastinate about almost anything that they do not habitually do. The process of doing almost any necessary task is then necessarily emotional, stressful and unpleasant, because each necessity of life brings with it a rising tide of negative emotions, which only recede when the action is eventually forced.”

“It has often been observed that a depressed person will suffer from compulsive, selfdefeating negative thoughts and feelings…The major problem is that negative thoughts, beliefs and ‘depressogenic assumptions’ are, once again, only symptoms of the underlying problem.”

“I am not an expert on depression, but, after all, it is happening in my own head and who knows more about what’s happening in my own head than I do?”

Dr. Youssef goes on to describe some very simple techniques that helped him break the autopilot habit, take charge of his life, and resolve his long-standing depression.

Dr. Youssef’s concepts resonated with me for three reasons.  Firstly, in both my personal and professional endeavors, I have always emphasized the need to take charge of one’s life vs. drifting along with the tide.  Secondly, Dr. Youssef’s ideas are a form of self-help, and represent an excellent counterpoint to the inherently dependence-inducing medical model.  Thirdly, psychiatry often confuses cause and effect.  It is psychiatry’s position that extreme depression causes indecisiveness; Dr. Youssef’s contention is that extreme indecisiveness causes depression.

Anyway, please take a look.  It’s a simple program with no costs, adverse effects, or downsides.  I would be interested in any feedback.

Antidepressant Drugs and Suicide Rates

In 2010, Acta Psychiatrica Scandinavica published a study by Göran Isacsson et al.  The paper was titled Antidepressant medication prevents suicide in depression.  Here’s the conclusion:

“The finding that in-patient care for depression did not increase the probability of the detection of antidepressants in suicides is difficult to explain other than by the assumption that a substantial number of depressed individuals were saved from suicide by postdischarge treatment with antidepressant medication.”

It’s a complicated article, with some tenuous logic, but note in particular the contrast between the fairly cautious wording in the conclusion, and the bold, even brazen, assertion in the title.

But, in any event, it’s all moot, because the article was retracted by the authors and by Acta Psychiatrica Scandinavica about sixteen months after publication.  The retraction had been requested by the authors because of “…unintentional errors in the analysis of the data…”

The research in question was conducted in Sweden.  Dr. Isacsson works at the Division of Psychiatry in the Karolinska Institutet, Stockholm.  He has been writing since at least 1994 on the putative efficacy of antidepressants in the prevention of suicide.

The 2012 retraction notice did not attract as much attention as the original article, but it did stimulate a measure of discussion.  Mickey Nardo wrote posts on the subject, here, here and here.  Bob Fiddaman wrote a post here, and Ivan Oransky of Retraction Watch wrote on the matter here.  Ivan reported that he had contacted Dr. Isacsson and Acta Psychiatrica Scandinavica for more information, and received the following reply from Dr. Isacsson:

“We discovered lately that there was a coding error regarding diagnoses in the database we utilized for the 2010 paper. When corrected, antidepressants were detected in depressed suicides as often as could be expected and not less than expected which was the crucial finding in the paper. This means that no conclusion can be drawn from the study regarding antidepressants’ effects on suicide risk in any direction.

The database has not been used for other studies so no other papers are affected.”

Jan Larsson, a Swedish journalist, wrote an interesting article on the matter.  Here’s an extended quote: 

“Isacsson’s findings from 2010 were widely published in Swedish newspapers, with headlines like  ‘Antidepressants prevent suicide’ (Dagens Nyheter), where it was said: ‘He [Isacsson] means that many become provoked to hear that depression is a deadly disease and that suicides can be prevented with medicines’. And, said Isacsson: ‘Therefore, it is important to show that antidepressants actually prevent suicide.’

In June 2012 I made an FOI request to Karolinska Institutet (where Isacsson is working) to get the corrected figures in this research project. I specifically wanted to get the document containing the correct percentage of antidepressants for those ‘who committed suicide and who had previously been treated at a psychiatric clinic for depression’ (the earlier mentioned group of 1077 persons).

The answer from Karolinska Institutet: This is confidential information, no data can be released.

It took a five month legal process to get access to the correct data. During this whole process Karolinska Institutet claimed that all the data in this research project were confidential.

In a final statement to the court, after having to answer specific questions, Karolinska Institutet stated that the correct figures did not exist at the time of the FOI-request – remember that they were said to be confidential at the time – but that the correct figures now had been produced.

Karolinska Institutet stated to the court: ‘that information has now been produced … The result shows that ‘the correct percentage’ is 56, meaning that of the persons who had been treated for depression in psychiatric care in the last five years before suicide, 56% had antidepressants in their blood when they committed suicide.’

So finally we got to know that the 15.2% in actual fact was 56% – an increase of 268% (from 164 persons to 603).

We had a seven pages long scientific article, with great impact in media, where doctors and the public got the message that antidepressants protect against suicide – an article built on Isacsson’s faulty finding that only 15.2% in the group had antidepressants in their blood when they committed suicide. And so the correct data, which completely defeated Isacsson’s speculations and conclusions in the original article, ‘published’ in a short statement to the court in Stockholm, where no doctor, no patient and no other researcher could find it.”

So, Dr. Isacsson et al’s original finding of 15.2% was a very large error indeed.  As I mentioned earlier, the logic underlying the study is tenuous, but Table 1 from the study will provide some insight into the authors’ thinking.

Isacsson Table 1

The controls (34,165) are people who did not commit suicide.  These are individuals who died from accidental and natural deaths.  Antidepressants were detected in 6.5% of these individuals post-mortem.

The suicides (18,922) represent all Swedish suicides from 1992 to 2003.  Antidepressants were detected in 22.4% of these people post-mortem.

Then the authors broke the numbers down further.  They note that 11,226 of the suicides had no psychiatric hospitalization in the 5 years prior to their deaths.  Of these individuals, 14.8% had antidepressants detected post-mortem.  The remaining 7,696 suicides, who had been in a psychiatric hospital in the preceding 5 years, had an antidepressant detection rate of 33.6%.

And this is where it gets complicated.  The researchers broke the hospitalized numbers down further, into:

  • Those hospitalized for depression only                              15.2%
  • Those hospitalized for other problems                               37.3%
  • Those hospitalized for depression plus other problems    33.2%

Their argument was that the first group (depression only) would be expected to have about the same, or an even higher, level of detected antidepressants as the other groups.  But, contrary to expectations, they found that they had the lowest level – about the same, in fact, as the group who had not been hospitalized in the previous five years.

So, they reason that large numbers of the hospitalized-for-depression-only group, most of whom presumably had antidepressants in their blood stream, had “been saved from committing suicide by antidepressant treatment.”

But as mentioned earlier, there was an error in the data, and the correct number was 56%.

Now all of this is well-known, but there is an aspect of the matter that has not, to my knowledge, been addressed previously.  Let’s go back to Dr. Isacsson’s letter to Retraction Watch.

“We discovered lately that there was a coding error regarding diagnoses in the database we utilized for the 2010 paper. When corrected, antidepressants were detected in depressed suicides as often as could be expected and not less than expected which was the crucial finding in the paper. This means that no conclusion can be drawn from the study regarding antidepressants’ effects on suicide risk in any direction.

The database has not been used for other studies so no other papers are affected.”

Dr. Isacsson is saying that antidepressants were detected in the depression-only suicides “as often as could be expected and not less than expected.”

Strictly speaking this is true.  56% is not less than 15%.  But the statement is also deceptive, in that 56% is a great deal more than 15%.  The difference in the study in question is 439 people.

Dr. Isacsson issued the above statement on March 19, 2012.  At that time, neither he nor Karolinska Institutet had released the 56% figure (on the patently spurious grounds of confidentiality).  It took several more months of legal process before the 56% figure was produced.  So at the time that Dr. Isacsson wrote  “…not less than expected…”, he probably did not anticipate that the true figure would ever be released.

But the plot thickens even further:

“This means that no conclusion can be drawn from the study regarding antidepressants’ effects on suicide risk in any direction.” [Emphasis added]

If a particularly low number (15%) warrants the conclusion in the article’s title (“Antidepressants medication prevents suicide in depression”), wouldn’t it be reasonable to infer that a particularly high number (56%) might warrant the opposite conclusion?  This is particularly so in that the increase from 15% to 56% can only have come at the expense of one or other of the remaining categories, which would make the discrepancy even larger.

I’m perfectly willing to accept that the original analysis was a genuine error.  But at the time of the retraction and the letter to Retraction Watch, Dr. Isacsson must have known that the true figure was 56%, and the question needs to be asked:  Why did he not release the 56% figure voluntarily at the time of discovery?  In addition, it is difficult to avoid the conclusion that his letter to Ivan Oransky was deliberately deceptive.  Mickey Nardo puts the matter well:

“It would be easy to drift into a debate about the relationship between suicide and antidepressants and miss the point here, which is that medical opinion should follow science, not the other way around. It’s clear that Göran Isacsson is of the opinion that antidepressants should be given to decrease the incidence of suicide – he has an absolute right to express that opinion. But when Isacsson offers as proof of his opinion a published study of the Swedish public records, and it turns out that his data either is wrong, not to be found, or never existed in the first place, we have to conclude that Göran Isacsson is an ideologue and has no place in the psychiatric literature.”

At the time of writing the article in question, Dr. Isacsson had financial ties to Lundbeck, Eli Lilly, and GSK.


Dr. Isacsson not only continues to promote the notion that wider use of antidepressant drugs will prevent suicides, but he also calls routinely for the removal of the FDA’s black box warning on this matter (e.g.  here).

In June 2010, the British Journal of Psychiatry published a debate on the topic:  The increased use of antidepressants has contributed to the worldwide reduction in suicide rates.  Arguing for the notion were Dr. Isacsson and Charles L. Rich, MD, Professor Emeritus of Psychiatry, University of South Alabama; arguing against were Jon Jureidini, MD, child psychiatrist at the Women’s and Children’s Hospital, Adelaide, and Melissa Raven, PhD, Research Fellow at Flinders University. Adelaide.

The debate effectively discredits Dr. Isacsson’s position, and is well worth reading.

Recurring Depression

This post was submitted by a reader.I am 46 years old and have taken antidepressants (Lexapro, Paxil, now Zoloft) for 10 years.  But the reason I began taking them wasn’t due to my own need for relief from depression or anxiety.  It was actually an effort to improve my relationship with my husband at the time.  He suffered from depression and took medication, but said that I was overly critical, driven, intense, etc. and I think he was right.  But I was also young and immature, and am an engineer by profession.  I do have a critical thought process, no doubt.  We were mismatched from the start and separated not long after I started the medication, but have a 11 year old son together.  The divorce process, and going back to work full time as a single mom was difficult and stressful.  But after taking the Lexapro for over 4 years, I actaully began feeling lethargic and depressed and decided to stop taking it cold turkey.  Big mistake, I learned the hard way, and ended up on Paxil after a few months. Now I am having the same problem with the Paxil, and I really just want to get off the medication all together because I feel that it is causing the depression.  I was never depressed to begin with, but now I am!  After a couple of bad experiences with withdrawal symptoms from coming off the meds, I am really apprehensive about trying to taper off of them, but I want myself back, not this medicated, lethargic, irritable, unproductive person.  I was far from perfect, as my ex-husband made painfully clear, but I always had hope for a better future and energy to work for it.  I can’t help but feel that the meds have done more harm than good in my particular situation.  I just wonder if others have had similar experiences?  Thank you and best wishes in whatever you are searching for…

A Reader