Tag Archives: antidepressants

Antidepressant-induced Mania

It is generally recognized in antipsychiatry circles that antidepressant drugs induce manic or hypomanic episodes in some of the individuals who take them.  Psychiatry’s usual response to this is to assert that the individual must have had an underlying latent bipolar disorder that has “emerged” in response to the improvement in mood.

The problem with such a notion is that it is fundamentally unverifiable.  Psychiatry defines “bipolar disorder” by the presence of certain behaviors and feelings.  If a person meets these criteria, he/she is said to have bipolar disorder.  What immediately needs to be noted is that bipolar disorder, in common with psychiatry’s other “disorders” has no explanatory value.  To illustrate this, consider the following hypothetical conversation.

Parent:  Why does my son behave in these extreme ways?
Psychiatrists:  Because he has bipolar disorder.
Parent:  How do you know he has bipolar disorder?
Psychiatrist:  Because he behaves in these extreme ways.

The only evidence for the illness is the very behavior that it claims to explain.

As spurious as this is from a logical point of view, the notion of a latent bipolar disorder is even worse.

Why did my son become manic after starting on antidepressant drugs?
Because he had a latent bipolar disorder.
How do you know he had a latent bipolar disorder?
Because he became manic.

What psychiatry is doing here is applying their spurious explanation retrospectively Before the individual showed any signs of mania, he must have had bipolar disorder because he became manic at a later date.  But nobody could ever have verified that hypothesis, because the occurrence of a manic or hypomanic episode is the primary criterion for such a “diagnosis”.

Although the “latent bipolar disorder” is psychiatry’s usual explanation for these episodes, one occasionally encounters acknowledgement that the antidepressant was the primary causative factor, and in practice, the two conflicting theories exist side by side.

  1. The manic/hypomanic episode was caused by the antidepressant drugs.
  2. The episode was caused by the underlying latent bipolar disorder.

Theory 2 is more popular in psychiatric practice, and is routinely told to those clients who experience this kind of mood switching.  Up till now it has been difficult to challenge theory 2, because it is essentially unassailable.  One can’t prove or disprove the existence of something that is inherently latent.

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

But recently some evidence has been published that favors theory 1:  that the manic/hypomanic episodes stem primarily from the antidepressant drugs.  In November 2013, Psychiatric Times published an article by Ross Baldessarini, MD, a Harvard psychiatrist, et al titled ‘Switching’ of Mood From Depression to Mania With Antidepressants.  

The article reports on, and discusses the implications of, a meta-analysis conducted by the same authors (Antidepressant-associated mood-switching and transition from unipolar major depression to bipolar disorder: A review, Baldessarini RJ, et al, Journal of Affective Disorders, May 2013).  Here’s the opening paragraph of the Psychiatric Times article.

“Bipolar disorder often presents initially with one or more episodes of major depression, and an episode of mania or hypomania may first occur during treatment with an antidepressant, stimulant, or other agent with mood-elevating effects. Such ‘switching’ of mood into mania, a mixed-state, or psychosis can be dangerous. This switching is particularly prevalent among juveniles and young adults exposed to treatment with an antidepressant or stimulant for a depressive, anxiety, or attention disorder. Such pathological shifts of mood and behavior may represent adverse drug actions or a manifestation of undiagnosed bipolar disorder.”

The authors go on to state that they had reviewed available research on two topics:  a) antidepressant-associated mood switching; b) changes of diagnosis from unipolar depression to bipolar disorder.

They identified 51 studies involving nearly 100,000 individuals who had been diagnosed with major depressive disorder (MDD) without a history of mania or hypomania, and who had been treated with an antidepressant.  They found that mood switching (i.e. to mania or hypomania) occurred in 8.2% of participants within an average of 2.4 years of antidepressant use, or 3.4% per year.  (The rate of mood switching was 4.3 times greater among juveniles than among adults.)

The authors also reviewed 12 other studies in which individuals who were initially considered to have unipolar depression (MDD),  were assigned a new diagnosis of bipolar disorder because of the occurrence of spontaneous (i.e. no antidepressant associated) mania or hypomania.  These switches occurred in 3.3% of the individuals studied within 5.4 years, i.e. 0.6% per year.

So, manic or hypomanic episodes were 5.6 (3.4 ÷ 0.6) times more likely per year for people diagnosed with MDD who were taking antidepressants than for people with the same diagnosis who were not taking these drugs.

The authors’ comments on this difference in the Psychiatric Times article are interesting:

“A particularly intriguing finding was the large apparent excess of antidepressant-associated switching over reported spontaneous diagnostic changes to bipolar disorder. This raises questions about the diagnostic, prognostic, and therapeutic implications of antidepressant-associated reactions.”

“If the relatively low rates of new bipolar diagnoses are not due to under-reporting, their marked difference from rates of antidepressant-associated mood switching leaves open the possibility that direct pharmacological, mood-elevating actions of antidepressants may be involved in mood switching, in addition to hypothesized “uncovering” or perhaps even “causing” of bipolar disorder. Of particular concern is that these ambiguous possibilities leave specifically uncertain the potential value of long-term treatment with antimanic or putative mood-stabilizing agents.”

In the Journal of Affective Disorders article, they also state:

“An important, unresolved question is of the significance of AD-associated mood-switching. Two plausible possibilities are:  [a] responses reflecting the presence of BPD, or [b] a direct pharmacological effect of mood-elevating treatments that may be transient, relatively rapidly reversible, and not followed by a change in diagnosis…The several-fold higher proportion of patients with mood-switches among unipolar MDD patients than the rate of later re-diagnoses of BPD is consistent with the possibility that some AD-associated mood-switches may represent pharmacologic reactions (AD-induced mania).  It is also likely that AD-associated risk will be greater than spontaneous mood-elevations regardless of cause. It is important to note that the reported rates of re-diagnosis to BPD may be somewhat overestimated if some cases involve drug-related mood-elevation and not only spontaneous mania–hypomania. That is the ratio of AD-associated mood-elevations to new diagnoses of BPD may actually be even higher than we found.” [Emphasis added]

What the authors are pointing out here is that antidepressants are clearly implicated in the “excess” incidents of mania/hypomania, and they have even raised the question of a direct causal link.

Their brief reference to “diagnostic…implications” isn’t entirely clear, but is, I think, a challenge to the DSM-5 decision to allow these kinds of antidepressant-induced manic episodes to count towards a “diagnosis of bipolar disorder.”

In DSM-IV, incidents of this kind were excluded:

Note:  Manic-like episodes that are clearly caused by somatic antidepressant treatment (e.g., medication, electroconvulsive therapy, light therapy) should not count toward a diagnosis of Bipolar I Disorder.”  (p 332) [Emphasis added]

But in DSM-5, this has been changed to:

Note:  A full manic episode that emerges during antidepressant treatment (e.g., medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the physiological effect of that treatment is sufficient evidence for a manic episode and therefore, a bipolar I diagnosis. (p. 124) [Emphasis added]

So under DSM-5, the possibility that the mania was caused by the antidepressant has been eliminated in favor of the popular psychiatric notion that it “emerged” during the antidepressant use, and the manic episode can be adduced to support a “diagnosis of bipolar disorder.”  This is psychiatric spin of a very advanced order:  eliminating the DSM-IV admission that the drugs have the potential to inflict this kind of damage, while at the same time expanding the concept of bipolar disorder, which is good for business.

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

But, here come Dr. Baldessarini et al collating and publishing research, some of which, incidentally, has been around since the late 60’s/early 70’s, clearly establishing a large excess of manic episodes among people taking antidepressant drugs.  And, notably, they have taken the additional step of writing up their findings in Psychiatric Times, a medical trade publication written for “psychiatrists and allied mental health professionals who treat mental disorders”, with a circulation of 40,000.

And, perhaps most significant of all, is Dr. Baldessarini et al’s reference to “prognostic and therapeutic implications.”

“Indeed, it is not even proved that drugs considered to be mood-stabilizing are highly protective against antidepressant-associated mood switching, although such protection is widely assumed.  Moreover, there is very limited evidence that prolonged antidepressant treatment provides substantial protection against recurrences of bipolar depression and that it might contribute to emotional instability or rapid cycling.”

In other words, in cases where antidepressant-associated manic episodes have occurred, continued use of antidepressants “might contribute” to instability and rapid cycling, i.e., recurrent manic episodes.

. . . . . . . . . . . . . . . . 

There has been an increasing recognition on this side of the debate that the so-called antidepressant drugs precipitate manic, and even violent, reactions, in some of the individuals who take them.  There has even been speculation that use of these products is linked to the much-publicized incidents of murder-suicide in recent years.  Brian, at AntiDepAware, has amassed a great deal of anecdotal, but compelling, information on this issue.  Joseph Glenmullen, MD, a psychiatrist, has discussed antidepressant-linked mood switching in his book Prozac Backlash  (2000).  He describes several cases from his practice, including individuals who became floridly psychotic, sometimes with graphically violent themes , after taking SSRI’s.

Psychiatry has resisted suggestions to conduct a definitive study on this matter, relying instead on repeated dogmatic assertions that the “meds” are wholesome and necessary, and that the incidents are the result of “untreated mental illness.”

But the Baldessarini et al study and, incidentally, an earlier Offidani et al study of which Dr. Baldessarini was a co-author, represent a major assault on that notion.  Tragically neither article appears to have attracted much attention in the psychiatric field, where antidepressants are still being prescribed routinely as front line “treatment” for depression and various other “disorders”, and no major alert with regards to mood-switching has been issued..  I have no inside information on this matter, but it occurs to me that Dr. Baldessarini et al have written the Psychiatric Times piece in an attempt to disrupt this complacency, and to generate some recognition among their colleagues of the enormous implications of antidepressant-induced manic episodes.  But perhaps their efforts have been in vain.  It is now 14 months since the publication of the Psychiatric Times piece, and 19 months since the original journal article, but no major change in psychiatric prescribing is evident, and psychiatrists are still telling victims of this effect that they must have had an “underlying bipolar disorder”, that the drug has activated.  As I’ve said many times, psychiatry does not take kindly to criticism.  And this appears to be true even when the criticism is from one of their own.

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Disclaimer:  In writing this post I have used terms like “bipolar disorder”, “major depressive disorder”, etc., in order to describe the journal articles being reviewed.  This was simply a reflection of the fact that the authors had used these terms, and should not be read as an indication of any endorsement on my part of the validity or usefulness of these terms.  Indeed, it is the central tenet of this site that the so-called psychiatric diagnoses have neither explanatory nor predictive validity, and are destructive, disempowering, and stigmatizing.

Mass Murderers and Psychiatric Drugs

There’s an interesting article in the current issue of the National Psychologist written by David Kirschner, PhD, a New York psychologist.  The National Psychologist is a newspaper-type magazine that publishes articles of general interest to psychologists and others working in this field.  Most issues contain a mix of opinion pieces, news, changes in government regulations, etc…

Dr. Kirschner’s article is titled Mass shooters received only limited treatment. 

Here are some quotes:

“As a forensic psychologist, I have tested/evaluated 30 teenage and young adult murderers, and almost all of them had been in some kind of ‘treatment,’ usually short term and psychoactive drug-oriented, before they killed.”

“After each episode of school killings or other mass shootings, such as the Aurora, Colo., Batman movie murders and Tucson, Ariz., killing of six and wounding of Rep. Gabrielle Giffords and 12 others, there is a renewed public outcry for early identification and treatment of youths at risk for violence.

Sadly however, most of the young people who kill had been in ‘treatment,’ prior to the violence, albeit with less than successful results.”

“Most of the young murderers I have personally examined had…been in ‘treatment’ and were using prescribed stimulant/amphetamine type drugs before and during the killing events. These medications did not prevent but instead contributed to the violence by disinhibiting normal, frontal cortex control mechanisms.”

“Prior to the violent event, for which he is currently serving a life without parole sentence, Jeremy [Strolmeyer], an honor student with no history of violence, was misdiagnosed with attention deficit hyperactivity disorder (ADHD) and ‘treated’ with nothing more than a bottle of Dexedrine following a brief 20-minute ‘cost-effective’ psychiatric consultation.”

“And so, despite ongoing congressional debates regarding stricter gun control laws vs. improved access to mental health treatment, our concern should be about the quality of mental health care, not just a societal safety net insuring treatment for all children and young adults. Almost all of them are covered by some type of managed care or insurance company, and the issue is not access to preventive treatment. The real problem, in my opinion, is the quality and competence of therapy for potential violent offenders when insurance companies are the gatekeepers.”

Obviously it’s a compelling article, particularly Dr. Kirschner’s assertion that “almost all” 30 young murderers he has worked with had been in some kind of treatment and had been taking psychiatric drugs.  Dr. Kirschner’s call for more competent and more intensive therapy makes sense, but as long as the mental health system is dominated by psychiatrists and psychiatric dogma, it is likely that psychiatric drugs will continue to be the essential ingredient of these interventions.  And as long as this is the case, all that we can reasonably expect is more of the same.

Dr. Kirschner’s comments are, of course, anecdotal. But there is an ever-growing body of anecdotal information implicating psychiatric drugs in mass killings and suicides. There is a desperate need for a formal study of this matter, but calls for such studies have been routinely ignored and resisted.

In December 2012, a petition on the White House “We the People” website calling for the government to initiate such an investigation was removed without explanation, even though it was well on the way to receiving the requisite number of signatures.

And let us not forget what Patrick B. Kwanashie, Assistant Attorney General for the State of Connecticut, said on this matter on August 22, 2013 when he was pressed in a freedom of information meeting to release Adam Lanza’s history of psychiatric drug use.

“…you have to advance reasons that you actually do have a real interest in the…medical records.  The plaintiff, the complainant have not shown any such interest.  The complainant is proposing that they can make generalizations, generalized from one single incident, no matter how the outcome of the use of antidepressants, or the causal link between the use of antidepressants and the kind of violence that took place in Newtown.  You just can’t, that’s not a legitimate use of that information.  You can’t generalize just from one case.  Even if you can conclusively establish that Adam Lanza’s murderous actions were caused by antidepressants, you can’t logically from that conclude that others would commit the same actions as a result of taking antidepressants.  So it’s simply not legitimate, and not only is it not the use to which they are proposing to put the information not legitimate, it is harmful, because you can cause a lot of people to stop taking their medications, stop cooperating with their treating physicians, just because of the heinousness of what Adam Lanza did.  As the material, the FDA material that they submitted show, it would take a lot of studies over a long period of time and among, and within various demographic groups to even begin to establish causal links between antidepressants and aggressive actions or suicidal behavior.  And the informed opinion has not quite reached the point to say definitively that there’s a causal link between the use of antidepressants and violent behavior.  Having correlations, there are correlations, but to say there are correlations doesn’t necessarily mean the relationship is causal.  And this is an issue the FDA is still grappling with, and so far it’s been willing to do is ask the drug makers to put warnings on their products and to advise physicians, treating physicians, to follow monitor their patients closely at the beginning of the taking of antidepressants.  So it’s a complex issue, and to pretend that you can just, based on this one case, make recommendations as to how people should make judgment choices is a disservice to the public and illustrates why these types of reports should not be made available, because in the wrong hands they can be the source of mischief.” [Emphasis added]

In other words, psychiatric drugs are safe until proven dangerous.  And, apparently, the only acceptable evidence is a large scale, randomized, controlled trial.  But the only group who has the data and the resources to conduct such a trial is psychiatry-pharma!  And meanwhile we should cover up any anecdotal information that might cast the drugs in a bad light – because that might induce people to stop taking them!

Psychiatric drugs are not medications in any meaningful sense of the term. Whatever temporary lift they may give people in the short term, is offset by their adverse effects – particularly their contribution to suicides and murder.

Information on this issue is being spun and suppressed by psychiatrists, and by their moneyed collaborators in pharma.  How much longer must this destructive charade continue?

More Bogus Conclusions From More Bogus Research

Robert Findling, MD, is a pediatrician and a psychiatrist.  He is the Director of Child and Adolescent Psychiatry at Johns Hopkins Children’s Center, and Vice President of Psychiatric Services and Research at the Kennedy Krieger Institute.

On July 31, Dr. Findling published a brief video (and article) on Medscape:  Adverse Events Caused by a Drug Warning?

Dr. Findling’s article is essentially a commentary on a study by Christine Lu et al, which was published by the BMJ on June 18.  Here is the conclusion paragraph from the Lu et al report:

“Safety warnings about antidepressants and widespread media coverage decreased antidepressant use, and there were simultaneous increases in suicide attempts among young people. It is essential to monitor and reduce possible unintended consequences of FDA warnings and media reporting.”

The Lu et al study was fundamentally flawed from various perspectives, and was widely criticized.  I did a critique of the paper here.  In that critique, I expressed the belief that the Lu et al study was never meant to be about science.  Rather:

“It was about spin and PR.  Its purpose was to attack and embarrass the media in order to keep them in line.  The fundamental message in the study, and in the NIH press release, is:  If you reporters print bad things about antidepressants, this will lead to reduced usage of these products, which in turn will lead to more suicides, and you will have blood on your hands!  Psychiatry is intellectually and morally bankrupt.  It has no valid response to its critics and is increasingly resorting to this kind of spin and PR.”

In fact, to their credit, the mainstream media did not pick up the Lu et al study to any marked degree, though the NIH, who funded the study, did issue a very misleading, and at times blatantly false press release.

But, back to Dr. Findling’s article.  Dr. Findling confined his observations to the adolescents (10-17) in the study.  Here are some quotes from his article interspersed with my comments.

“What did the study find? First, there was a 31% reduction in the rate of antidepressant prescriptions. Second, there was an increase of 21% in the rate of psychotropic drug poisonings in adolescents.”

This statement is false.  Here’s the passage from Lu et al:

“We estimated a relative reduction of 31.0% in antidepressant use in the second year after the warnings…At the same time as the substantial reduction in antidepressant use, we observed a sharp increase in psychotropic drug poisonings (fig 1). We estimated a significant relative increase of 21.7% in psychotropic drug poisonings in the second year after the warnings…”

The key word in this last quote is “estimated,” which appears twice.

Lu et al did not, as Dr. Findling asserts, find a 31% reduction in the rate of antidepressant prescriptions, nor did they find a 21% increase in the rate of psychotropic drug poisonings.  Rather, Lu et al estimated these numbers.

They graphed antidepressant use and psychotropic drug poisonings for 1.1 million adolescents who were enrolled in a consortium of group insurance plans.  The data was graphed from 2001 (q.1) to 2010 (q 4).  The black box warnings were mandated by the FDA in October 2004.

From the 2001 (q 1) to 2003 (q 3) data, Lu et al calculated trend lines for antidepressant use and for drug poisonings.  They excluded from this trend analysis the period 2003 (q 4) to 2004 (q 4) on the grounds that this was a phase-in period for the warnings.

They extended these trend lines for the second half of the study period, as shown in the diagram below.  The orange dotted lines are the trend line extensions.

Fig 1 Lu et al




Adolescents (10-17)










They chose the last quarter of 2006 (i.e. two years after the mandated black box warnings) as a reference point and calculated that at that point, antidepressant use was down 31.0%.  But these changes were not calculated against the actual data at the time of the warnings.  They were calculated against Lu et al’s trend line estimates of what would have been the case in 2006 (q 4) had the data continued to trend in the same direction, and at the same rate.  Here’s Lu et al’s statement on the matter:

“…we also provided absolute and relative differences (with 95% confidence intervals)…in the second year after the warnings (that is, in the last quarter of 2006), which were estimated by comparing the overall changes in outcome attributable to the warnings with counterfactual estimates of what would have happened without the warnings.” [Emphasis added]

In reality these kinds of short-term trend lines are notoriously unreliable, and the notion of assessing a percentage change against what might have been the case is fraught with potential for error.  And incidentally, I’m not familiar with the term “counterfactual,” but Merriam-Webster’s Collegiate Dictionary (2009) gives “contrary to fact” as the definition.  So perhaps Lu et al were trying to tell us something!

What the data, for this particular group of adolescents, actually shows is that antidepressant use did decrease beginning about a year before the black box warnings.  It is likely, but not certain, that this decrease was related to the publicized suicidality concerns, the FDA advisories, and the FDA warnings.  But psychotropic drug poisonings remained relatively flat (with some fluctuations) from the beginning of the study until about the beginning of 2008.  At that point the graph starts to climb.

A critical point here is that one can manipulate trend lines readily by choosing the start and finish points for one’s study period.  There is nothing  in the Lu et al data to support an association (much less a causal link) between the reduction in antidepressant use that started in 2003 (q 4) and the increase in drug poisonings that started about the beginning of 2008.  And even if these two variables were perfectly correlated, in the absence of additional evidence, there would be no reason to believe that the adolescents who didn’t take the antidepressants were the same individuals who were hospitalized for drug poisoning.

. . . . . . . . 

Back to Dr. Findling:

“The purpose of the current study was to examine 3 key variables during the second year after the FDA warnings were issued:

• Rate of antidepressant prescriptions;

• Rate of psychotropic drug poisonings (which can serve as an indicator of suicide attempt rate); and

• Rate of completed suicides.”

Despite the cautious wording in the second item, there is a clear implication that psychotropic drug poisonings (ICD-9 code 969) can be used as a substitute, or proxy, measure of suicide attempts.  In my earlier post, I drew attention to the fact that drug poisoning is only one method of committing suicide, and in many cases is not a suicide attempt, but rather an accidental overdose.  I also pointed out that ICD-9 code 969 includes poisonings by caffeine, marijuana, amphetamines, and Ecstasy, overdoses of which are not, to my knowledge, often used as methods of suicide.

Here’s what Lu et al say on this matter:

“…instead of deliberate self harm E-codes, we used poisoning by psychotropic agents (international classification of diseases, ninth revision, clinical modification (ICD-9 code 969), a more reliable proxy for population level suicide attempts.33 34

Reference 34 is to an earlier Lu et al study, on the completeness of deliberate self-harm (E-codes) in commercial insurance plan databases.  So the only reference cited in support of using drug poisonings as a proxy measure for suicide attempts is reference 33.  This is a 2010 paper by Patrick et al.  On July 14, less than a month after the publication of Lu et al, the BMJ published a letter from Catherine Barber, Matthew Miller (two of the authors in Patrick et al) and Deborah Azrael, all of Harvard School of Public Health.  Here’s a quote from their letter.

“Lu et al used poisonings by psychotropics (ICD-9 code 969) as a proxy for suicide attempts in claims data from 11 health plans, in spite of the fact that the code covers both intentional and unintentional poisonings. Our paper, which is the sole reference to their claim that code 969 is a ‘validated’ proxy for suicide attempts, in fact shows that in the U.S. National Inpatient Sample the code has a sensitivity of just 40% (i.e., it misses 60% of discharges coded to intentional self-harm) and a positive predictive value of 67% (i.e., a third of the discharges it captures are not intentional self-harm).”

And, in reference to other studies cited in Barber et al’s letter:

“On balance, the evidence shows no increase in suicidal behavior among young people following the drop in antidepressant prescribing. It is important that we get this right because the safety of young people is at stake. Lu et al’s paper sounding the alarm that [suicide] attempts increased was extensively covered in the media. Their advice that the media should be more circumspect when covering dire warnings about antidepressant prescribing applies as well to their own paper.” [Emphasis added]

So, the very people that Lu et al were citing to support their use of drug poisonings as a proxy measure of suicide attempts, have not only repudiated this methodological decision, but have also cited evidence contradicting Lu et al’s primary finding.

. . . . . . . . 

Back to Dr. Findling:

“An accompanying editorial [in the BMJ]…commented that the net effect was that the FDA warning led to more harm.”

This is an accurate reflection of the content of the editorial in question, which was written by John Geddes, Professor of Psychiatry at Oxford University; Andrea Cipriani, Senior Clinical Researcher, also at Oxford Department of Psychiatry; and Rob Horne, Professor of Behavioral Medicine, University College London.  Here’s what they wrote:

“The net effect of the warning was probably counterproductive and led to more harm.”

In fact, for the reasons given above, there is nothing in the Lu et al data to even suggest that the warnings “led to more harm.”

But Geddes et al went on to distort the facts further:

“Completed suicide is such a rare event that even this large observational study lacked the power to investigate this outcome.”

There is a subtle implication here that the warnings did lead to an increase in completed suicides, but that the Lu et al study lacked the power to detect this.  In fact, the Lu et al study did have the power to detect fluctuations in the suicide rate, and did investigate this specific outcome.  Lu et al stated very clearly:

“Our study was the first to examine the effects of the warnings on completed suicides over a long period. In contrast with the increases in suicide attempts, even with large sample sizes we observed no changes in suicides after the warnings. Completed suicides are rare; only one tenth as common as suicide attempts. Nevertheless, our data are consistent with the Centers for Disease Control and Prevention report that showed gradual increases in completed suicides between 1999 and 2010, without sudden discontinuities around the time of the FDA warnings and media reports, among people aged 10-34 years…”


“Completed suicides did not change for any age group.”

The Geddes et al editorial, copied dutifully by Dr. Findling, is a scandalously deceitful piece of psychiatric propaganda.

. . . . . . . . 

And finally, from Dr. Findling:

“The data from this study suggest that adverse events not only can occur from medicines but also as a result of warnings. This leads to the unanswered question: How do we communicate treatment-related outcomes and treatment-related concerns effectively and openly to ensure improved patient outcomes without unwanted consequences?”

In reality, the only significant consequence of the warnings emerging from the Lu et al study pertaining to adolescents (10-17) is a reduction in the use of antidepressant drugs in this particular group.  There is no evidence of an increase in psychotropic drug poisonings, suicide attempts, or completed suicides.

The essential dynamic in all of this is that the FDA’s warnings, which incidentally were long overdue, had a negative impact on pharma-psychiatry’s image, and on their business, but had no negative impact on client welfare.  Nevertheless, psychiatry continues to resist the reality that their sacred drugs do in fact cause harm, and that the FDA warnings were needed.  For psychiatry, business and professional status routinely trump client welfare.

Psychiatry is morally and intellectually bankrupt.  They have never had any intelligent or logical response to the criticisms that are being leveled against them, including the well-established fact that their so-called antidepressant drugs induce suicidal feelings and actions in some people, particularly children and young adults.  They refuse to accept this because it contradicts their dogma.  Instead, they use spin, propaganda, and fear-mongering to promote their drugs.


Dr. Findling, according to his Johns Hopkins bio,

“…has been honored with numerous awards and has received both national and international recognition as a clinical investigator.”

And  yet, he apparently couldn’t see the flaws in the Lu et al study, even though these flaws have been widely publicized.  This is indeed puzzling, but becomes clearer as one continues with his bio:

“Findling is currently the principal investigator on an NICHD contract that is comprehensively examining lithium in the treatment of pediatric mania. In addition, he is the principal investigator of an NIMH study that is assessing the longitudinal course of children with manic symptoms. He is also the site principal investigator of an NIMH-supported clinical trial that is examining the treatment of children with severe aggression. His research is also supported in part by the Stanley Medical Research Institute and the pharmaceutical industry.”

Antidepressants and Overall Wellbeing

There was an interesting article published on April 12, 2014 in Psychotherapy and Psychosomatics.  It’s called The Efficacy of Antidepressants on Overall Well-Being and Self-Reported Depression Symptom Severity in Youth: A Meta-Analysis, by Gary Spielmans and Katherine Gerwig, both of the Psychology Department, Metropolitan State University, St. Paul, Minnesota.

The authors conducted a word-search in Medline, PsychINFO, and the Cochrane Central Register, and identified 8 studies that met their criteria.  They combined the data from these studies and concluded:

“Though limited by a small number of trials, our analyses suggest that antidepressants offer little to no benefit in improving overall well-being among depressed children and adolescents.”

In the Discussion section of the paper, they stated:

“We found no evidence that antidepressants offer any sort of clinically meaningful benefit for youth on self-report measures of depression, quality of life, global mental health, or parent reports of autonomy.”

The authors acknowledge that their study has limitations,  “…the most obvious being the small sample of included trials.”

“A larger sample of relevant trials may lead to differing conclusions.  However, even the strongest signal of efficacy in our results (a pooled statistically nonsignificant effect of g = 0.16 across measures of autonomous functioning, self-esteem, global mental health, and quality of life among adolescents) provides little reason to suspect any robust treatment effects.”

The article goes on to discuss the relative merits of self-report vs. practitioner ratings as measures of efficacy in antidepressant trials:

“Given the high emphasis on clinician-rated depression measures in the reporting of clinical trial outcomes and subsequent reviews…it seems that even the modest efficacy found in prior antidepressant meta-analyses is inflated.  Perhaps this is best illustrated by fluoxetine [Prozac].  The discord between small to moderate effect sizes on clinician-rated measures in three trials (0.52, 0.60, and 0.40)…and negligible to quite modest effects on self-reports (-0.07, 0.22, and 0.15) is notable.  Further, the only fluoxetine trial to report quality of life and global mental health outcomes found no treatment benefit.”


“It is unclear exactly how different outcome measures should be weighed, but our findings suggest that the overall benefits of antidepressants in youth have been overstated and that their overall benefit over placebo may be vanishingly small.”

And more disturbingly:

“…a recent systematic review found a much elevated risk of excessive arousal/agitation among youth taking antidepressants versus placebo…Data from a Food and Drug Administration systematic review also found that antidepressants were linked to a statistically significantly higher rate of hostility or agitation relative to placebo…Clearly, a more expansive examination of the risk-benefit ratio of antidepressants in youth, extending beyond clinician-rated depression measures and suicidality, is needed.”

. . . . . . . . 

The first review mentioned in the above quote is Offidani E. et al, 2013.  Here’s their conclusion:

“Risks of excessive mood elevation during antidepressant treatment, including mania-hypomania, were much greater than with placebo, and similar in juvenile anxiety and depressive disorders. Excessive arousal-activation in children or adolescents treated with antidepressants for anxiety as well as depressive disorders calls for particular caution and monitoring for potential risk of future bipolar disorder.”

The FDA review mentioned is the 131 page review by Tarak Hammad, MD, PhD on the link between suicidal behavior and antidepressants’ in youth.  On the link to hostility/agitation, Dr. Hammad stated:

“Although none of the individual trials had a statistically significant result, the overall RR [risk ratio] for Paxil and the overall RRs for all drugs and for all SSRIs were statistically significant showing an increase in the risk of developing these symptoms in the drug group as compared to the placebo group.”

. . . . . . . . 

Perhaps it’s time to stop calling these drugs antidepressants.


I found no links to the Spielmans, Gerwig article in the mainstream media.  In fact, I found only two outlets that picked it up:  MinnPost, where I found it, and MDLinx.  MinnPost is  “…a non-profit, nonpartisan enterprise whose mission is to provide high-quality journalism for news-intense people who care about Minnesota.”  MDLinx is an online newsletter that  “…aggregates medical articles and research from more than 1,200 peer-reviewed journals and leading news media on a daily basis.”

Suicidal Behavior After FDA Warnings

On June 18, the British Medical Journal published an article by Christine Lu et al, titled Changes in antidepressant use by young people and suicidal behavior after FDA warnings and media coverage: quasi-experimental study

Here’s the conclusion paragraph from the abstract:

“Safety warnings about antidepressants and widespread media coverage decreased antidepressant use, and there were simultaneous increases in suicide attempts among young people. It is essential to monitor and reduce possible unintended consequences of FDA warnings and media reporting.”

Note the slightly rebuking tone directed against the FDA and the media.


The researchers interrogated the claims databases (2000-2010) of eleven medical insurance groups who collectively cover about 10 million people in 12 geographically scattered US locations.  All groups were members of the Mental Health Research Network (MHRN).

The general concept behind this sort of research network is that computerized insurance claims data represent an enormous repository of potentially very useful information, which researchers can readily tap for answers to questions that are difficult to resolve with smaller-scale data.  MHRN’s website, under the tab “Funding“, states:

“Initial funding for the MHRN is through a 3-year cooperative agreement with the National Institute of Mental Health (U19 MH092201 “Mental Health Research Network: A Population-Based Approach to Transform Research”) and through a supplement from NIMH to the existing Cancer Research Network funded by the National Cancer Institute.

During the initial funding cycle, the MHRN developed core infrastructure for collaborative research and conducted four developmental research projects to test and leverage that infrastructure in specific clinical areas.”

The Lu et al study is one of these four projects.

MHRN’s “virtual data warehouse” contains information on inpatient and outpatient treatment, and outpatient pharmacy data.  It also contains, for deceased members, the date and cause of death.

The present study included all adolescents (10-17), young adults (18-24), and adults (20-64) in the eleven insurance groups.


From the pharmacy data, the authors calculated the quarterly percentages of individuals who were dispensed an antidepressant.

The frequency of suicide attempts was measured by the quarterly incidence of “poisoning by psychotropic agents,” (ICD-9 code 969), that resulted in inpatient or ER treatment.

The frequency of completed suicides per 100,000 members was also calculated quarterly.  Although the other data elements are presented for each quarter up to the end of 2010, the completed suicide data stops at the end of 2008.  The authors explain:  “There is generally a lag time of 12-24 months for both reporting of deaths and availability of data; therefore we analyzed data on deaths up to and including 2008.”


The study’s time frame was from the first quarter of 2000 to the last quarter of 2010.  The researchers divided this time frame into three segments:

1.  The pre-warning phase (2000, q1 – 2003, q3)
2.  The phase-in period (2003, q4 – 2004, q4)
3.  The post-warning period (2005, q1 – 2010, q4)

The FDA black box warnings were mandated in October 2004.

The authors justify the use of a phase-in period as follows:

“To deal with the possibility of an anticipatory response to the warnings, we considered the last quarter of 2003 to the last quarter of 2004 as a ‘phase-in’ period that spanned the entire period of FDA advisories, the boxed warning, and intense media coverage, and excluded these five data points from the regression models.”

Regression, in this context, basically means finding a line-of-best-fit through a series of points which represent data on a graph.


The study included approximately the following numbers of individuals:

Adolescents (10-17)                1.1 million
Young adults (18-29)              1.4 million
Adults (30-64)                            5    million

The results for the three age groups are set out in graph form and are designated Figures 1, 2, and 3.

Let’s start with the adolescent graphs (Fig 1)

Fig. 1 Rates of antidepressant use, psychotropic drug poisonings, and completed suicides per quarter before and after the warnings among adolescents enrolled in 11 health plans in nationwide Mental Health Research Network

Fig 1 Lu et al



Adolescents (10-17)












The graph is divided into three parts.  The upper part shows antidepressant use, quarter by quarter, for the period of the study (2000, q1 – 2010, q4).  Each dot represents the percentage of the 1.1 million adolescents that were taking antidepressants in that particular quarter.  So in the first quarter of 2000, a little over 1.5%  were taking the drugs, and so on.

The middle part of the figure shows the percentage of adolescents who were treated for psychotropic drug poisoning in each quarter.

And the lower part shows the number of completed suicides (per 100,000) in the group, plotted quarterly, and graphed as a continuous line (the dark green line) rather than as dots.  The lighter lines represent the 95% confidence interval.  In other words, the chances are 95% that the true suicide rate for the population lies between these lines.

The slightly darker vertical band that goes up through the middle of all three graphs is the phase-in period (2003, q 4 – 2004, q4).  The solid lines in the upper and middle sections are the regression lines for the pre and post warnings data.  The post lines are curves because the authors report that this fitted the data better.  The orange dotted lines in the post area are simply the projection of the pre-warning regression lines; i.e. a projection of what purportedly would have happened if the warnings had not been issued.  Completed suicide data for the last two years of the study was not available.

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

The data for the young adults (Fig 2) is presented similarly.

Fig 2 Rates of antidepressant use, psychotropic drug poisonings, and completed suicides per quarter before and after the warnings among young adults enrolled in 11 health plans in nationwide Mental Health Research Network

Fig 2 Lu et al


Young Adults (18-29)












The data for older adults is shown in Fig. 3


Fig 3 Rates of antidepressant use, psychotropic drug poisonings, and completed suicides per quarter before and after the warnings among adults enrolled in 11 health plans in nationwide Mental Health Research Network 

Fig 3 Lu et al


Older Adults (30-64)













The FDA warnings were not aimed at adults.  The authors state that the adults were included in the study  “…as a ‘control’ group.”

From all of this data, the authors draw the following results/conclusions:

1.  The FDA safety warnings, plus the media coverage, “decreased antidepressant use.”

2.  There were simultaneous increases in suicide attempts by young people.

3.  It is essential to monitor “unintended consequences” of black box warnings and media reporting.

4.  Completed suicides did not change for any group.

The main thrust of the article is expressed in the final paragraph:

“Undertreated mood disorders can have severe negative consequences. Thus, it is disturbing that after the health advisories, warnings, and media reports about the relation between antidepressant use and suicidality in young people, we found substantial reductions in antidepressant treatment and simultaneous, small but meaningful increases in suicide attempts. It is essential to monitor and reduce possible unintended effects of FDA warnings and media reporting.”

Again, we see the rebuking tone aimed at the FDA and the media.


As mentioned earlier, the study was funded by the National Institute of Mental Health (NIMH), which is a division of the US National Institutes of Health (NIH).  The study was published on June 18.  On June 19, NIH issued a two-page press release via its own website, Medline Plus.

Here are some quotes from the press release, interspersed with my comments and observations.

“Teen suicide attempts rose nearly 22 percent after the U.S. Food and Drug Administration (FDA) warned about dangers of antidepressants, a new study finds.”

This statement is false.  What the study found was that within the HMO Research Network’s insurance plans in ten states, psychotropic drug poisonings (including, incidentally, according to the press release, poisonings by marijuana, amphetamines, and Ecstasy), that required medical treatment, rose by the stated amount.  This is only one method of attempting suicide, and in many cases might not be attempted suicide at all.  The study provided no information on the incidence of confirmed suicide attempts measured as such.  Incidentally, ICD-9 code 969, which Lu et al used as a proxy measurement for suicide attempts, also includes “poisoning by caffeine”!

The statement is also misleading, in that the changes in the rates of psychotropic poisonings were measured not against the previous rate of poisoning as is implied in the above quote, but against the projected rate, based on the 2000 – 2003 regression line.  This is critical because regression lines can be extraordinarily poor predictors, as any stock market analyst can attest.

Regression lines are also easy to manipulate by the simple expedient of delineating the time boundaries to show a desired trend.  In the present study, for instance, the exclusion of the phase-in data from the pre-warning regression analysis definitely had the effect of lowering the poisoning trend projection in the young adult group (Fig 2), and probably had this effect in the adolescent group (Fig 1).  Excluding the phase-in data from the regression analysis was an arbitrary decision.  The researchers might just as readily have used a simple pre-post cutoff based on the quarter in which the warnings were mandated.

It is also noteworthy that the percentage changes in antidepressant prescriptions and psychotropic poisonings were assessed solely on the 4th quarter of 2006.  The authors’ statement on this matter is interesting:

“In addition, we also provided absolute and relative differences (with 95% confidence intervals)…in the second year after the warnings (that is, in the last quarter of 2006), which were estimated by comparing the overall changes in outcome attributable to the warnings with counterfactual estimates of what would have happened without the warnings.”

Note the unwarranted causal implication (“attributable”), and the assumption that the authors knew what would have happened had the warnings not been issued.  “Counterfactual” according to my Webster’s means “contrary to fact”.  I’m not sure what the authors had in mind in describing their projections this way.

There is also, I think, a suggestion in the above quote that the result applies to the general population.  This, however, would only be the case if in fact the group of individuals studied had been selected at random from the US population.  This is emphatically not the case.  The study group comprised all the individuals between ages 10 and 65 who were enrolled in the eleven MHRN insurance groups in the 12 states..  This group, for instance, is certainly not representative of uninsured people, nor of people in other locations.

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

“Following the warnings, antidepressant prescriptions for young people fell by more than a fifth. At the same time, suicide attempts rose, possibly because depression was being undertreated, according to background information in the study.”

This statement is false.  What the study found was that antidepressant prescriptions for adolescents (10-17) declined from a peak of about 1.9% in 2003, q3 to a low of about 1.3% in 2008, q2, and then climbed to about 1.7% in 2010, q 3 (Fig 1).  But the figures for young adults (18-24), who are presumably included in the term “young people” as used above, remained remarkably constant at about 4% from 2004, q1 to 2010, q4.  The only “fall” for this group is a notional fall from the trend line. (Fig. 2)

Again in this quote, we see the implied causal link to suicide attempts, and even a suggested explanation:  “possibly because depression was being undertreated.”  The study provides no information on general nationwide trends in the frequency of suicide attempts, and even if suicide attempts were trending upwards during the period in question, there are many other possible explanations.  Also in this quote we see the invalid substitution of the term “suicide attempts” for psychotropic drug poisonings.

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

“‘We found a substantial reduction in use of antidepressants in youth, and also in adults — who were not targeted by the warning,’ said lead author Christine Lu, an instructor in population medicine at the Harvard Pilgrim Health Care Institute in Boston.”

Here again, this statement is false.  The antidepressant use data for young (Fig 2) and older (Fig 3) adults remained almost perfectly flat in the post-warning period.  As noted earlier, the only falls were from the projected trend lines.

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

“Lu attributes the drop in prescriptions to the FDA’s warning and resulting media coverage. ‘To a certain extent, the FDA’s black box warning was legitimate, but the media emphasis was really on suicide without noting the potential risk of undertreatment of depression. Because of that, there has been an overreaction, and that overreaction has sent alarming messages to parents and young people,’ she said.”

Note the skilful tightrope walking.  Dr. Lu and the NIH want to bash the media for publicizing the link between antidepressants and suicidal activity, but at the same time not overly antagonize the FDA.  The media ignored the “potential risk of undertreatment”; the media overreacted; the media caused alarm.  Big bad journalists need to get into line!

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

Then we have a truly magnificent piece of psychiatric spin:

“Although the initial studies showing an increased risk of suicide in teens taking antidepressants prompted the black box warnings, researchers never proved that the medications were the cause of the increased risk of suicide, only that there was a link.

Likewise, though the current research finds a strong association between the uptick in suicides and the drop in antidepressant use, Lu and her colleagues weren’t able to definitively show that a decrease in antidepressant prescriptions was directly responsible for the recent increase in suicide attempts.”

The deliberations and the data on which the FDA black box warnings were based were comprehensive, and showed a clear link between antidepressant use in young people and suicidal activity.  And the evidence was sufficient to convince the FDA to take action.

The findings in the Lu et al study do not come even close to this standard.  But by counterposing them in this way, the NIH is trying to convey the impression that the findings of the present study are comparable in quality to the earlier work.

Note also the blatant falsehood:  “…the current research finds a strong association between the uptick in suicides and the drop in antidepressant use…”  [Emphasis added] In fact, the Lu et al study found no increase in completed suicides.  They stated clearly in their abstract:  “Completed suicides did not change for any group.”

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

“Coverage of the warning may have had unintended consequences, Lu said. Doctors may have been less willing to prescribe antidepressants and parents may have been fearful of letting their children take them, she said.

The lesson, Lu said, is that the media and the FDA should strive for the right balance so potential overreactions don’t occur.”

Again, big bad media needs to get in line and print only what psychiatrists tell them to print (“the right balance”).

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

“Undertreating depression is worse than the slight increase in suicidal thoughts antidepressants may cause, Lu said. ‘It’s also a reminder for doctors to weigh the risk of a drug with the risk of not treating or undertreating the condition,’ she said.”

This is extremely misleading.  Note how the concerns on which the boxed warnings were based are dismissed:  “…the slight increase in suicidal thoughts antidepressants may cause.”

The pediatric meta-analysis data on which the FDA deliberated in 2003-2004 are written up in detail (131 pages) here.  Tarak Hammad et al published the formal journal report in 2006.  It is clear that great pains were taken to include in the primary outcome measure only adverse events that had clear suicidal potential.  The primary outcome, which was labeled “suicidal behavior or ideation”, contained three elements:

  • Suicide attempts, and/or
  • Preparatory actions towards imminent suicidal behavior, and/or
  • Suicidal ideation

The overall risk ratio (drug vs. placebo) for the three elements combined was found to be 1.95 (95% CI, 1.28 – 2.98).  The risk ratio for suicidal behavior (first two items) was 1.90 (95% VCI, 1.00 – 3.63).  In other words, the individuals in the studies who took the drug were about twice as likely to have made a suicide attempt, and/or made preparations for imminent suicide, and/or had been actively thinking about suicide than those who took the placebo.  This is emphatically not something to be dismissed as “a slight increase in suicidal thoughts…”

Hammad et al acknowledged the limitations of their study, but went on to state:

“Despite the limitations, the observed signal of risk for suicidality represents a consistent finding across trials, with many showing RRs [risk ratios] of 2 or more. Moreover, the finding of no completed suicides among the approximately 4600 patients in the 24 trials evaluated does not provide much reassurance regarding a small increase in the risk of suicide because this sample is not large enough to detect such an effect.”

They also provide the following interpretation of their findings:

“…when considering 100 treated patients, we might expect 1 to 3 patients to have an increase in suicidality beyond the risk that occurs with depression itself owing to short-term treatment with an antidepressant.” [Emphasis added]

In addition, since the issuing of the black box warnings in 2004, there have been two studies confirming the link between suicidal activity and antidepressants.

Olfson et al 2006 found:

“…in children and adolescents (aged 6-18 years), antidepressant drug treatment was significantly associated with suicide attempts (OR [odds ration], 1.52; 95% CI, 1.12-2.07 [263 cases and 1241 controls]) and suicide deaths (OR, 15.62; 95% CI, 1.65-infinity [8 cases and 39 controls]).”

And Olfson et al 2008 found:

“Among children, antidepressant treatment was associated with a significant increase in suicide attempts (odds ratio [OR] = 2.08, 95% confidence interval [CI] = 1.06 to 4.10; cases, N = 51; controls, N = 239; p = .03).”


The Lu et al article, and the authors’ conclusions, received wide coverage in the general media. Most of the mainstream media simply regurgitated the gist of the study plus the press release with additional quotes from two of the authors, Christine Lu, PhD, and Steven Soumerai, ScD, both from Harvard’s Department of Population Medicine.

Both the Washington Post and The Boston Globe delivered the authors’ message pretty much without reservation.  Here’s a quote form the Washington Post:

“…Wednesday’s study wrote that while the government’s actions in 2003 and 2004 were legitimate and thorough, ‘FDA advisories and boxed warnings can be crude and inadequate ways to communicate new and sometimes frightening scientific information to the public.’ Likewise, researchers argue that while media attention can create much-needed awareness…sometimes ‘the information may be oversimplified and distorted when communicated in the media.'”

And from The Boston Globe:

“The study’s authors say that patients and doctors, frightened by news coverage that exaggerated the risk of antidepressants, shunned treatment that might have prevented the suicide attempts.”

In fact, there is no information in the report as to whether the victims of the poisonings had taken antidepressants or not.

And amazingly,

“Steven B. Soumerai, a coauthor and a Harvard professor of population medicine, said black box warnings typically have little effect on physician behavior, unless they are accompanied by news reports.”

In his attempt to castigate the press for publicizing the black box warnings, has Dr. Soumerai inadvertently shot psychiatry in the foot?  Do psychiatrists actually pay more attention to news reports than to FDA warnings?

Bloomberg also ran the standard story:

“A widely publicized warning by U.S. regulators a decade ago about risks for teenagers taking antidepressants led to plummeting prescriptions and increased suicide attempts, Harvard University researchers said.”

Note the clearly implied causality (“led to”), the exaggeration (“plummeting”) and the mischaracterization of psychotropic poisonings as “suicide attempts.”

“‘After the widely publicized warnings we saw a substantial reduction in antidepressant use in all age groups,’ said Lu, an instructor in population medicine at Harvard Pilgrim Health Care Institute, in a telephone interview. ‘Warnings, especially widely publicized warnings, may have unintended consequences.'”

“Lu said the focus by the media on the risk of suicide, even though the review of data found no increase in completed suicides, frightened patients and parents.”

Again, the big bad media frightening patients and parents.

But Bloomberg also obtained some rebuttal quotes from Marc Stone, MD, a senior medical reviewer at the FDA:

“‘It’s a stretch to say that the people that are committing suicide or the increase in suicide attempts has to do with the prescription of antidepressants,’ Stone said in a telephone interview. ‘There’s absolutely nothing in the study to say that these are the people who would have been prescribed the antidepressants if it weren’t for the warnings.'”

“There are other issues that could be influencing the drop in antidepressant prescription and rise in poisonings, Stone said. The data presented in the study shows a steady increase before the warnings in antidepressant prescription rates for adolescents while drug poisonings remained relatively steady. The rise in poisonings after the warnings when prescriptions declined slightly in that group doesn’t show a link between the two events, he said.

‘They’re describing a very strange phenomenon in society that’s supposedly being held back by antidepressant use,’ Stone said. ‘It doesn’t stand up to what we know about the mental health situation in the United States.'”

I could find nothing in the New York Times, the Wall Street Journal, or the LA Times about the study or the press release.

Medscape, a web resource for physicians and other health professionals, toed the party line:

“The safety warnings were covered widely in the media and led to a decrease in antidepressant use by young people, but at the same time, there was an increase in suicide attempts, Christine Y. Lu, PhD, of the Department of Population Medicine, Harvard Medical School in Boston, Massachusetts, and colleagues found.”

Again, note the inaccurate characterization of drug poisonings as “suicide attempts”.

“The researchers say that it is possible that the warnings and extensive media attention led to ‘unexpected and unintended population level reductions in treatment for depression and subsequent increases in suicide attempts among young people.'”

And the focus on the “extensive media attention”.

The APA drew attention to the Lu et al study in a Psychiatric News Alert, but the tone of the piece was appropriately and, I must say, surprisingly, skeptical.  The only quote was from Mark Olfson:

“Mark Olfson, M.D., M.P.H., a professor of psychiatry at Columbia University Medical Center and an expert in mood disorders, told Psychiatric News that ‘the new findings shed little light on the complex associations between anxiety and depressive disorders, antidepressant treatment, and the risk of self-harm and suicide. The measure of suicide attempts used in this study, psychotropic poisonings (ICD-9 code 969), is only loosely related to suicide attempts. Most suicide attempts in young people do not involve poisoning by psychotropic drugs and most intoxications do not represent suicide attempts.’

Because of the recent substantial increase in unintentional poisonings from stimulants, Olfson stated that the increase in psychotropic overdose could be a result of an underlying substance use disorder rather than suicide. ‘This trend [of psychotropic overuse by youth], which may be driven by complex societal factors, deserves study and clinical attention,’ Olfson concluded.”

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

Finally, the most reasonable interpretation of the Lu et al data is that following the black box warnings, the long-standing increase in the use of antidepressant drugs was halted, but suicide rates remained about the same (N = 7.5 million).


This is not the first attempt to discredit/undermine the black box warnings for these drugs.  In September 2007, Robert Gibbons, PhD et al published Early evidence on the effects of regulators’ suicidality warnings on SSRI prescriptions and suicide in children and adolescents in the American Journal of Psychiatry.  The paper was based on a study of US and Dutch SSRI prescription rates to children and adolescents from 2003 to 2005, and was funded by NIMH grant.  The authors reported the following results:

“SSRI prescriptions for youths decreased by approximately 22% in both the United States and the Netherlands after the warnings were issued. In the Netherlands, the youth suicide rate increased by 49% between 2003 and 2005 and shows a significant inverse association with SSRI prescriptions. In the United States, youth suicide rates increased by 14% between 2003 and 2004, which is the largest year-to-year change in suicide rates in this population since the Centers for Disease Control and Prevention began systematically collecting suicide data in 1979.”

And drew the following conclusions:

“In both the United States and the Netherlands, SSRI prescriptions for children and adolescents decreased after U.S. and European regulatory agencies issued warnings about a possible suicide risk with antidepressant use in pediatric patients, and these decreases were associated with increases in suicide rates in children and adolescents.”

The report contains a graph showing a sharp increase in suicide rates for children and adolescents (5 – 19) between 2003 and 2004.

Gibbons Fig 2

The data for this graph was extracted from the CDC WONDER Compressed Mortality Database (up to 2002) and from the CDC WISQARS Injury Mortality Report Database (2003 – 2004).  On the face of it, this graph does seem to show a dramatic increase in completed suicides for this age group between 2003 and 2004.  But when we look at the bigger picture, this trend is not so obvious.

On July 1, I extracted completed suicide rate and population data from the CDC website for the period 1979 to 2010.  The Gibbons et al graph is for ages 5 – 19.  I was unable to obtain that graph from the CDC site, but I was able to collate the raw data and draw the graph using Excel software.  Here’s the graph:

Suicides per 100,000, 1979-2010

As can be readily seen, the increase in the suicide rates for this age group from 2003 to 2004 does not appear as marked or as noteworthy when viewed against the wider background.  Drawing conclusions from short-term trends is fraught with potential for error.  Dr. Gibbons et al were obviously aware of these issues, and provided a lengthy discussion/argument in support of the relevance of the associated trends.  Nevertheless, here’s their closing paragraph:

“In December 2006, the FDA’s Psychopharmacologic Drugs Advisory Committee recommended that the black box warning be extended to cover young adults, and in May 2007, the FDA asked drug manufacturers to revise their labels accordingly. If the intent of the pediatric black box warning was to save lives, the warning failed, and in fact it may have had the opposite effect; more children and adolescents have committed suicide since it was introduced. If as a result of extending the black box warning to adults there is a 20% decrease in SSRI prescriptions in the general population, we predict that it will result in 3,040 more suicides (a 10% increase) in 1 year (17). If the FDA’s goal is to ensure that children and adults treated with antidepressants receive adequate follow-up care to better detect and treat emergent suicidal thoughts, the current black box warning is not a useful approach; what should be considered instead is better education and training of physicians.”

The Washington Post ran an article on the Gibbons et al study, Youth Suicides Increased As Antidepressant Use Fell, September 6, 2007.  The article included the following quotes:

“Thomas Insel, director of the National Institute of Mental Health, said, ‘We may have inadvertently created a problem by putting a ‘black box’ warning on medications that were useful.’ He added, ‘If the drugs were doing more harm than good, then the reduction in prescription rates should mean the risk of suicide should go way down, and it hasn’t gone down at all — it has gone up.'”

“The trend lines do not prove that suicides rose because of the drop in prescriptions, but Gibbons, Insel and other experts said the international evidence leaves few other plausible explanations.” 

Given the behavior of the trend line since 2004, these quotes suggest, at the very least, an over-reaction from the authors and from the NIMH.  And the fact that the NIMH funded both studies suggests that they may have an agenda:  to promote antidepressant drugs as safe, and to downplay any indications to the contrary.

If the NIMH genuinely wants to explore the sources/causes of suicide, they need to recognize three facts:

1.  Suicide is a complex, psychosocial phenomenon, and its roots/causes vary enormously from individual to individual, and from community to community.  Psychiatry routinely asserts that the root, or major cause, of suicide is depression, but this assertion is meaningless because suicidal activity/rumination is one of psychiatry’s defining features of depression.  A genuine understanding of human actions involves so much more than assigning labels.

2.  The facts surrounding any completed suicide are always, by the nature of the matter, at least partially hidden.

3.  Any attempt to understand suicide must involve a detailed, open-minded exploration of individual cases.  Variables that appear associated with suicide trend lines provide, at best, suggestions that might inform these explorations, but can also be very misleading.


At the present time, there is a great deal of anecdotal information, on the Internet and elsewhere, to the effect that individuals who were not previously suicidal, became so, shortly after starting SSRI’s.  The psychiatrist Joseph Glenmullen drew attention to this graphically and convincingly in Prozac Backlash (2000).  Here’s a quote:

“…the key elements in these stories appeared to be the ‘dramatic change’ observed in these people after starting Prozac, how ‘out of character’ their behavior was on the drug, and the often extraordinary degree of violence not only toward themselves but toward others.”

Elsewhere in the book, Dr. Glenmullen makes it clear that his comments apply, not only to Prozac, but to all drugs in the SSRI category.  Psychiatrist Peter Breggin has made similar points.  AntiDepAware has accumulated an enormous amount of anecdotal information on this matter.

Psychiatry tends to dismiss these kinds of concerns as “anecdotal”.  In this context, “anecdotal” usually means:  based on casual or incidental information rather than on systematic observations and evaluations.  In particular, the term suggests a subjective, rather than an objective approach.

But in fact, the raw data for virtually all psychiatric research is anecdotal in this sense.  If a person reports suicidal ruminations after taking an SSRI, this is anecdotal.  But if a study participant reports that he’s feeling better after taking an SSRI, this is also anecdotal.  And if 20 people make essentially similar statements, that’s 20 anecdotal statements.  And if they make these statements by answering 17 questions on the Hamilton Rating Scale for Depression, then we have 340 anecdotal statements.  The fact that the HDRS-17 is widely used, and yields numerical data which can be collated into rows and columns and analyzed with sophisticated computer programs doesn’t alter the fact that the raw data is anecdotal.

No one on this side of the issue is suggesting that a large proportion of people taking antidepressant drugs kill themselves.  If that were the case, then the drugs would have been removed from the market long ago.  What is being contended, however, is that these drugs are inducing strong suicidal urges in a relatively small proportion of individuals who had not previously had thoughts of this kind, and that some of these people are succumbing to these urges, and are taking their own lives.  That is indeed anecdotal information.  But it’s also very important, and it warrants investigation even if it involves only a fraction of one percent of the people taking the drugs.  To dismiss these widespread and credible contentions on the basis of the dogmatic insistence that the drugs are wholesome, or that the individuals were probably suicidal to begin with, is simply unconscionable.  This is particularly the case in that firstly, the proof of the wholesomeness of these products is also, ultimately, based on anecdotal information, and secondly, there is no way to reliably identify the individuals concerned prior to prescribing the drugs.

Prescribing these psychoactive drugs is like playing Russian roulette with someone else’s life.  The notion that this information should be suppressed because it might scare people from taking the products is cruel, callous, and irresponsible.  Psychiatry’s persistent and self-serving efforts to suppress this information is a national, and indeed, worldwide, scandal.

The Lu et al study, and the NIH press release, reminds me of a statement made by Patrick B. Kwanashie, Assistant Attorney General in Connecticut, after the Adam Lanza murders/suicide:

“Even if you can conclusively establish that Adam Lanza’s murderous actions were caused by antidepressants, you can’t logically from that conclude that others would commit the same actions as a result of taking antidepressants.  So it’s simply not legitimate, and not only is it not the use to which they are proposing to put the information not legitimate, it is harmful, because you can cause a lot of people to stop taking their medications, stop cooperating with their treating physicians just because of the heinousness of what Adam Lanza did.”


The Lu et al study has been subjected to a great deal of criticism.  These criticisms have been cogent and valid, but there is also a bigger picture.  The Lu et al study was never meant to be about science.  It was about spin and PR.  Its purpose was to attack and embarrass the media in order to keep them in line.  The fundamental message in the study, and in the NIH press release, is:  If you reporters print bad things about antidepressants, this will lead to reduced usage of these products, which in turn will lead to more suicides, and you will have blood on your hands!  Psychiatry is intellectually and morally bankrupt.  It has no valid response to its critics and is increasingly resorting to this kind of spin and PR.

Organized psychiatry realizes that it has lost the present debate on its logical/scientific merits.  They realize that their only hope for survival as a profession hinges on their ability to control the media.  In the pursuit of this objective, there truly are no depths to which they will not sink.

Over the past two decades, I have become convinced of two things:

1.  SSRI’s, and possibly other psychiatric drugs, are inducing strong suicidal and violent urges in some people.
2.  This information is being systematically suppressed by psychiatry and by the NIMH.  To the extent that they acknowledge it at all, they pretend that this suppression is in the public interest.

If there was ever a time when we need courageous and well-informed reporting, it is now.  Let us hope that the press has sufficient integrity and courage to resist psychiatry’s tawdry blackmail, to follow the evidence, and to print the truth.   In this context, it is very encouraging that neither the New York Times, nor the LA Times, nor the Wall Street Journal took the Lu et al bait.

It is time to end the charade.  The link between psychiatric drugs and suicide/violence needs urgent study by independent, adequately funded investigators who are given access to all the information.

A Client’s Perspective on “Mental Illness”

A very important and compelling article was posted on Mad in America on June 18.  It’s by Andrew L. Yoder, and is called An Open Letter to Persons Self-Identifying as Mentally Ill.  Here are some quotes:

“My physician was not so cautious.  He was a very pleasant man that always seemed to take his time with me and did not talk down to me.  Yet as I described some of the emotional distress I was experiencing, and the ways it was affecting my life, he told me with great certainty that mine was a totally common experience.  He told me that I had a biological condition in my brain, one in which certain chemicals were ‘imbalanced.’  He told me that there should be no stigma about asking for assistance from him.  Specifically he told me, ‘Trying to not be depressed is like telling a diabetic to just make more insulin.’  He prescribed an antidepressant medication, saying that this was no different than taking medication to regulate blood pressure or manage cholesterol.  I was told of the likelihood that I would need to remain on some form of medication for an indefinite future.”

“I believe that anyone, given the right context and circumstances, can experience even the most extreme forms of cognitive and emotional distress.”

“However, I believe that treating the term ‘mental illness’ as a literal truth does more to harm that hope of recovery than it does to help it.  You see, along with the popular claim that mental illness is a literal organic brain disease ‘just like diabetes’ is a set of other dogmas unproven and unsupported by evidence.  These include, being regularly told that not only do you have a disease but that this disease also has no cure and that you will struggle with it for your entire life.  I have trouble imagining anything more hopeless than that.

It also includes being told that you must take psychiatric medications, and often many different psychiatric medications for the rest of your life, and you should never ever consider stopping them.”

“Looking back now, I wish the physician who prescribed me anti-depressants would not have told me stories of ‘chemical imbalance’ that are simply not based in science.  In truth, most psychiatric medications alter normal brain activity, and there’s no evidence of an identifiable chemical imbalance of any sort at the root of emotional suffering.  Research suggests that there are some risks associated with long-term use of antidepressants, including the possibility of decreasing benefits from the drug and something referred to as ‘treatment resistant depression.'”

“Those of us challenging the evidence-absent medical model and the objective ‘mental illness’ label that goes with it are not trying to take away something hopeful and healing from you.  Instead, we wish to counter the false-hopelessness of a system that sees you as second-class people who will never be ‘normal.'”

“We know that mental and emotional suffering is a real experience that many, many people face.  We also know that nothing good comes from convincing people that they have a biological disease when no evidence supports that.  Questioning the legitimacy of ‘mental illness’ doesn’t make the reality of the pain any different.  But it does help people avoid the pitfalls of misinformation and powerlessness in their own recovery and wellness.”

“I am not saying that you are not hurting.  I am saying that you are not broken.”

Andrew has managed to express, in candid yet empathic terms, so many of the issues that are central to this debate.  Please read and pass along.

Do We Underestimate the Benefits of Antidepressants?

On April 19, 2014, The Lancet published an article titled Do we underestimate the benefits of antidepressants by German psychiatrists Mazda Adli and Ulrich Hegerl.

The Lancet, founded in 1823, is a weekly, general medical journal which since 1991 has been owned by Elsevier, a private, Amsterdam-based, publishing house with offices in the UK, USA, and other countries.

The gist of the article can be gathered from the opening paragraph:

“In the past 5 years, doubts have been raised about the therapeutic effectiveness of antidepressants in patients with depressive disorders, because of the small differences in symptom improvement between antidepressants and placebo recorded in randomised controlled trials (RCTs). With the recent debates about lowering of disease thresholds in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition, and the medicalisation of normal bereavement, this scepticism has increased. For the large group of patients with mild depression, the differences between antidepressants and placebo are not thought to be large enough to be clinically significant—ie, at least three points on the Hamilton Depression Rating Scale, HAMD-17.1 Therefore, several guidelines…no longer recommend antidepressants as first-line treatment for patients with mild and moderate depression, and instead generally favour psychotherapy. We are concerned that scepticism about the benefits of antidepressants goes too far, and risks depriving many patients with depression of effective treatment.”

The authors argue that randomized controlled trials (RCT’s), as currently conducted, systematically underestimate the benefits of antidepressants and overestimate the benefits of psychotherapy.  They present six main arguments.

1. (a)  Trial participants who are actually taking the drug (as opposed to the placebo) have less hope/expectation of benefit, because they know that they might just be taking the placebo.

(b)  Participants who are actually taking the placebo have more hope of benefit, because they know that they might be taking the drug.

2.  One of the problems with RCT’s is that participants drop out for various reasons.  Most RCT’s deal with non-completers by assuming that their outcome status at the point of drop-out remains the same for the pre-determined period of the study.  This is known as the last observation carried forward (LOCF) technique, and can sometimes underestimate treatment efficacy, because the non-completers dilute the statistical impact of those participants who took the drug and, presumably, steadily improved for the entire period of the trial.

3.  Study participants may not mirror real-life patients.  The authors point out that the prospects of free treatment coupled with financial incentives could result in more “inappropriate and uncompliant” individuals being enrolled in studies than one would find in a typical psychiatric practice setting.

4.  In routine care, practitioners can change the drug and the dosage to meet the emerging needs of the individual, whereas this kind of creative modulation of treatment is often not permitted in RCT’s.

5.  Effect sizes in psychiatric RCT’s are comparable to many effect sizes in general medicine.

6.  The evidence base for psychotherapy is less solid than that for antidepressants.

All of these issues are interesting and debatable.  Any research that involves human activity, thoughts, or feelings is fraught with problems of definition, quantification, and procedures.  Questions can be difficult to formulate, and answers are seldom simple and clear.  Each of the authors’ contentions have been debated at length in the literature, and it is easy to offer counter-arguments.  For instance, with regards to the LOCF issue, it is true that in situations in which treatment is linearly correlated with improvement, LOCF does indeed underestimate treatment efficacy; but in a context in which treatment can also cause deterioration or adverse effects, LOCF can lead to overestimates of efficacy and underreporting of harm.

Similarly with regards to argument number 1 above, it is also widely recognized that a great many trial participants can tell whether they are taking the drug or the placebo – thereby increasing the placebo effect for those taking the drug.

Argument number 3 neglects to point out that the randomization process ensures that there are as many “inappropriate and uncompliant” participants in the placebo group as there are in the drug group.  That’s the purpose of randomization!  And so on.

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

But what’s interesting is that in all the years that pharma-psychiatry was churning out its fraudulent, spurious and self-serving “findings,” I never heard of a single complaint from psychiatry about these kinds of methodological issues.  Now that their drug “treatments” are being exposed as not quite the panacea that they had claimed, they cry “foul!”

It’s also interesting that the article focuses solely on the relative merits of antidepressants vs. psychotherapy, but makes no reference to the much more serious problem – that long-term ingestion of antidepressants is the primary cause of what psychiatry in characteristically self-exculpatory fashion calls treatment resistant depression.

This article is not about science.  It is not, as it purports to be, a discussion of scientific methodology.  A genuine discussion of the six points listed above would have presented both sides of the coin, and many such genuine discussions have been published in the past 50 years, not only in mental health, but in general medicine and other fields.  The Adli and Hegerl article is PR and marketing, and this becomes clear in the final paragraph:

“In summary, the present approach to estimation of the benefits of antidepressant treatments is likely to underestimate the clinical significance of antidepressants and overestimate that of psychotherapy. At the same time, we are experiencing an increasing tendency to medicalise individuals who have emotional reactions to difficult life circumstances but without any clinical signs of depression, and to offer them antidepressants or psychotherapy which might not be appropriate to their needs.…We should be careful not to offer our treatments to the wrong patients, but to provide them consistently to the right patients.”

Note particularly the second sentence:  “… to medicalise individuals who have emotional reactions to difficult life circumstances but without any clinical signs of depression…”

This is just a rewording of the old psychiatric chestnut:  that depression-the-illness is fundamentally different in kind from depression-the-ordinary-feeling-that-we-all-get-when-we-experience-a-loss-or when-life-isn’t-going-too-well.  This is one of the great psychiatric falsehoods because, in practice and in theory, the fact that a person’s depression might be an “emotional reaction to difficult life circumstances” has no bearing whatsoever on whether the individual is assigned a diagnosis, and is prescribed an antidepressant.  The widely-used term “clinical depression” crystallizes this falsehood by creating the impression that such an entity exists (after all, it has a name!), and is fundamentally different from ordinary, everyday depression.  The implication in the authors’ apparently benign and sensible injunction is that psychiatrists should drug clients who have clinical depression, but not those whose depression is merely an emotional reaction to “difficult life circumstances.”

But it’s a meaningless recommendation, because there is no “diagnosis” in the DSM-5 chapter on Depressive Disorders that contains an exclusion clause based on the fact that the depression is a reaction to difficult life circumstances.  Indeed, the whole thrust of DSM and psychiatry for the past fifty years has been that if a person is significantly depressed – for any reason – this is diagnosable as a psychiatric “illness” and should be “treated” with drugs.    Even the tenuous two-month bereavement exclusion of DSM-III and IV has now been eliminated, as the authors themselves noted.

And in fact, DSM-5 specifically cautions practitioners not to rule out the possibility of a major depressive disorder in cases in which people are having understandable reactions to difficult life circumstances.  Here’s a quote from the Diagnostic Criteria section for Major Depressive Disorder (p. 161):

“Note:  Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural disaster, a serious medical illness or disability) may include the feelings of intense sadness, rumination about the loss, insomnia, poor appetite, and weight loss noted in Criterion A, which may resemble a depressive episode.  Although such symptoms may be understandable or considered appropriate to the loss, the presence of a major depressive episode in addition to the normal response to a significant loss should also be carefully considered.  This decision inevitably requires the exercise of clinical judgment based on the individual’s history and the cultural norms for the expression of distress in the context of loss.”

All that’s needed for a diagnosis to be made is a psychiatrist’s “clinical” and, incidentally subjective, judgment that the vague “diagnostic” criteria are met.

In addition, Axis IV (Psychosocial and Environmental Problems), which had provided practitioners an opportunity to at least identify relevant life circumstances, has also been eliminated.  Psychiatry’s old distinction of endogenous vs. exogenous depression didn’t die a natural death.  Rather it was systematically eliminated by the APA on the ground that it was irrelevant.

The authors’ final cautionary note – not to offer the pills to the wrong “patients,” but to provide them consistently to the right “patients” – is also a meaningless platitude, because within psychiatry’s diagnostic framework, there is no way of distinguishing these two groups on any dimension other than severity, and there is no reliable way of accomplishing even that.  In practice, the assessment of severity, and hence the status of the “diagnosis” is always a function of a practitioner’s subjective opinion, and, also in practice, the pills are given to virtually anyone who can be shoe-horned into a depression “diagnosis,” regardless of precipitating circumstances, which is precisely the state of affairs towards which pharma and organized psychiatry have striven for the past fifty years.


The article concludes with the following disclosure statement:

“MA [Mazda Aldi] has received grants or research support from Aristo, Servier, and Bristol-Myers Squibb; honoraria for speaking from Deutsche Bank, the Johanniter Order, East German Savings Banks Association, Pusch Wahl Legal Lawyers, HRM Forum, Helios Media, Lundbeck, Bristol-Myers Squibb, Boehringer Ingelheim, Servier, Aristo, Viiv, and Gilead; travel grants from the Alfred Herrhausen Society, Lundbeck, and Servier; and has been a consultant to Deutsche Bank, Bristol-Myers Squibb, Aristo, Merz, and Lundbeck. UH [Ulrich Hegerl] has received funding from health insurance companies (Barmer BEK, Central Versicherung); is or has been a member of advisory boards for Lilly Deutschland, Lundbeck, Otsuka, and Takeda, and has received honoraria for speaking from Bristol-Myers Squibb, Medice Arzneimittel, and Roche Pharma.”

Depression vs. Normal Unhappiness

Alex Langford is a British trainee psychiatrist.  He blogs at The Psychiatric SHO, and on April 21, he posted an article titled Antidepressants are not ‘happy pills.’  Thanks to Jean Davison for the link.

The article is an impassioned attack on psychiatry’s critics.  Here are some quotes, with my responses:

“I am sick and tired of the way the press portrays depression as unhappiness and antidepressants as ‘happy pills’.”

This is interesting, though my general impression is that the mainstream media lean a good deal more towards psychiatry than towards our side of the debate.  In addition, the words “depression” and unhappiness are pretty much synonymous.  So it’s difficult to see why that, or the characterization of antidepressants as “happy pills,” should be so upsetting to Dr. Langford.  We all, of course, have our linguistic likes and dislikes.  I personally don’t care much for the growing trend to pronounce the indefinite article as “ay,” or for psychiatry’s insistence on calling neuroleptic drugs “anti-psychotics.”  But what can you do?  I just Googled the phrase “antidepressants are happy pills” and got 204,000 hits!  So the notion has some traction and is probably here to stay.  One can’t legislate for the way people use words.  Or perhaps psychiatrists imagine that they can.

“For problems in other areas of health we’d only trust the experts to comment, but when it comes to mental health it seems like anyone can cast judgement.”

Ah.  Now it becomes clear.  We psychiatrists know what we’re doing, and how dare these ignorant upstarts “cast judgement” on our pronouncements!

Note also the implication that psychiatry is a medical specialty.  The fact is that people generally display more respect towards real doctors than they do towards psychiatrists, because real doctors deal with real illnesses.  Psychiatrists, by contrast, invent the “illnesses” that they treat, and then, with the help of their pharmaceutical allies, sell these illnesses and their “treatments,” with all the sophistication of door-to-door brush salesmen.

“Every author seems to think they’ve discovered something amazing, when all they’re actually doing is repeatedly insulting a huge group of people with their ignorance.”

Wouldn’t it be better to actually offer some counter-arguments, instead of this petty and undignified vituperation?

“Depression is not normal unhappiness, it is not something everyone goes through at some point. Only someone who has not been depressed would say that.”

This is a constant theme in psychiatry – that depression, the “illness,” is fundamentally different from ordinary, everyday depression.  But psychiatry has never offered any evidence to support this notion.  The much more reasonable position is that depression is depression is depression!  It admits of degrees, of course, but there’s not the slightest evidence that severe depression is a different kind of entity from moderate or mild depression.  In science, the burden of proof lies with the party making the extreme claim.  But psychiatry has never produced any proof; just repeated assertions.

“I agree, the causes and biological markers of depression are still murky to us. We don’t have a blood test or a scan for it and we realised that the ‘serotonin hypothesis’ was too simplistic decades ago. But this does not make depression any less of an illness, because the symptoms are still there. Just like migraines, we know very little, but we shouldn’t bizarrely stop calling it an illness just because of that.”

The biological markers of depression are not “murky.”  They are non-existent!  The causes of depression, in contrast, have been known from the beginning of history:  loss, disappointment, unfulfilling lifestyle, history of victimization, etc.  If by “we” Dr. Langford means the general body of psychiatry, then the question needs to be asked:  If psychiatry has known for decades that the chemical imbalance theory of depression was too simplistic, why was it only seven years ago (2007) that the Royal College of Psychiatrists removed all references to chemical imbalances from the depression section of their website?  And given that psychiatrists had promoted the notion avidly up to that point, why have they never published a recantation, and an apology to the people who were misled and harmed? 

Also, it needs to be stressed that the chemical imbalance theory is not just “too simplistic,” it is blatantly false.  It was developed as a tentative hypothesis by Everett and Toman in 1959, (Valenstein, Blaming the Brain, 1998, p 258) but never garnered sufficient evidence to warrant serious consideration.  The perpetuation of this discredited hypothesis as fact by psychiatry was not an honest mistake.  It was out and out, self-serving deception, and is likely to go down in history as one of the most destructive and far-reaching deceptions ever perpetrated by a professional body.

And then we have the great leap of faith:  “but this does not make depression any less of an illness, because the symptoms are still there.”  Actually, failure to identify an actual pathology does make a condition less of an illness.  In fact, it confirms the notion that it is not an illness at all.  For five decades now psychiatry has been telling us that depression is an illness “just like diabetes” and that the identification of the pathology is just around the proverbial corner.  Well, we’ve been round many corners, but the putative pathology has still not been identified.

“…because the symptoms are still there.”  This is pure chicanery.  Psychiatry, arbitrarily and self-servingly labels the natural indications of depression “symptoms.”  And now Dr. Langford is arguing back from this medical term to support the notion that depression is an illness!

And then, of course, we get the old migraine chestnut.  Yes, indeed, there are some real illnesses out there (including migraines) whose precise biological causes are unknown.  But in the great majority of real illnesses, the causes are known, and it is this knowledge of causes that has lifted general medicine from its folklorish roots to the respected and effective profession that it is today.  In psychiatric “illnesses,” by contrast, none of the putative biological causes are known, despite decades of heavily funded and highly motivated research.

I’m at a loss as to the significance of the word “bizarrely.”  Apparently Dr. Langford is saying that the proposition:  “Depression is not an illness” is bizarre!  Within psychiatric circles, the word “bizarre” is generally associated with delusions.  Is Dr. Langford suggesting that those of us who challenge psychiatry’s medicalization of depression are actually delusional?  Is there a hint of grandiosity here?

“For the final time:  Depression is not normal unhappiness and antidepressants are not ‘happy pills’.”

“For the final time…”  Yes, indeed, I think there is a touch of grandiosity here:  I – the great psychiatrist – have spoken, and that’s an end to it.  However, it will take a little more than Dr. Langford’s impassioned personal decree to lay this issue to rest.

Psychiatry has built an elaborate and multi-faceted structure; but it is built on spurious premises and bogus research.  The spuriousness and the destructiveness are being exposed daily, and psychiatry has no response other than to keep rolling out the same tired, unproven assertions.  Dr. Langford may be just a trainee psychiatrist, but he has certainly mastered the intricacies of psychiatric “logic,” in which falsehoods become truth by virtue of vigorous and widely promoted repetition.

Psychiatry is intellectually and morally bankrupt.  It’s finished!  The petulant protests of Dr. Langford are simply further confirmation that when all is said and done, psychiatry has no answer to its critics.


Antidepressants Make Things Worse in the Long Term

In June 2011, Rif El-Mallakh, MD, et al. published an article, Tardive dysphoria: The role of long term antidepressant use in inducing chronic depression, in Medical Hypotheses.  The article is a thorough and wide-ranging study review.

Here are some quotes from the abstract:

“Treatment-resistant and chronic depression appear to be increasing.”

“Depressed patients who ultimately become treatment resistant frequently have had a positive initial response to antidepressants and invariably have received these agents for prolonged time periods at high doses.” [Emphasis added]

The authors propose the term “tardive dysphoria” to describe this condition.  Tardive means delayed; dysphoria means unhappy or depressed.  The idea is that just as prolonged ingestion of neuroleptics causes tardive dyskinesia, so the prolonged ingestion of antidepressants causes tardive dysphoria.  It’s a nice idea, but the name hasn’t caught on – at least not yet.

The paper by Dr. El-Mallakh et al. is very detailed, and cites 85 references.  The arguments are well-marshaled and compelling.  Here’s a brief summary.

Depression affects about 5% of the world’s population.  Risk of recurrence is high (about 50-80%).  Maintenance antidepressant therapy may reduce the risk of relapse in the first year after an episode.  The APA recommends maintenance therapy for recurrent major depression.  But recurrence of depression is common even among individuals on maintenance therapy.  Recurrences of this sort are called treatment-resistant depression (TRD), the prevalence of which among depressed individuals may be as high as 30-50%.  This prevalence has increased from about 10-15% in the early 1990’s to about 40% in 2006.  Various reasons have been suggested for this increase, but, there “…are reasons to believe that antidepressant treatment itself may contribute to a chronic depressive syndrome.”

The authors provide a great deal of evidence in support of this conclusion.

“Up to 80% of patients diagnosed with major depressive disorder will experience a recurrence of depressive episode despite constant maintenance dose of an antidepressant.”

“Attempts to treat these individuals frequently result in poor response and the rise of TRD.”

“…there have been several reports of the loss of antidepressant efficacy.”

And perhaps most telling:

“A long-term placebo-controlled, blinded maintenance study of fluoxetine [Prozac] in major depression, found no difference after 62 weeks in subjects who were still euthymic [i.e. not depressed] on fluoxetine (11%) or placebo (16%).”

Dr. El-Mallakh et al. point out that individuals who were not initially depressed, but were given antidepressants for other problems (e.g. anxiety), often became significantly depressed.

“In a recent study 27% of patients without any history of a mood disorder who had received antidepressants for an average of 29 months for panic disorders, developed a cyclothymic illness that persisted for 1 year after antidepressant discontinuation.” [Emphasis added]

Also, and perhaps most alarmingly, it is stated:

“In…patients who have developed TDp [tardive dysphoria], ongoing attempts to treat the depression with antidepressants perpetuate the TRD, and may ultimately make the chronic depression permanent.”

The article was published in 2011, and the authors conclude their paper by calling for

“…blinded, randomized antidepressant discontinuation/continuation trials in TRD patients, over at least 1 year.”

They also suggest that

“…clinical trials of antidepressant taper and discontinuation for 6-12 months in patients who have failed most other options appear reasonable.”

Despite this call, I have not been able to find any follow-up research on this matter.

The notion that long-term ingestion of antidepressants leads to chronic, severe depression is not new. The present authors attribute the introduction of the concept to Giovanni Fava, MD, in his editorial Do antidepressant and antianxiety drugs increase chronicity in affective disorders?, Psychotherapy and Psychosomatics, 1994.

They also mention a paper by Verinder Sharma, MD, Treatment resistance in unipolar depression: Is it an iatrogenic phenomenon caused by antidepressant treatment of patients with a bipolar diathesis? Medical Hypotheses, 2006.

Dr. El-Mallakh himself and two other authors, Courtney Waltrip and Christopher Peters, wrote:  Can Long-Term Antidepressant Use Be Depressogenic? as a letter to the editor in the Journal of Clinical Psychiatry in 1999. 

In Anatomy of an Epidemic (2010), Robert Whitaker also addresses this issue (Chapter 8 – An Episodic Illness Turns Chronic).  Robert’s summary on this matter is clear and straightforward:

“We can now see how the antidepressant story all fits together, and why the widespread use of these drugs would contribute to a rise in the number of disabled mentally ill in the United States.  Over the short term, those who take an antidepressant will likely see their symptoms lessen.  They will see this as proof that the drugs work, as will their doctors.  However, this short-term amelioration of symptoms is not markedly greater than what is seen in patients treated with a placebo, and this initial use also puts them onto a problematic long-term course.  If they stop taking the medications, they are at high risk of relapsing.  But if they stay on the drugs, they will also likely suffer recurrent episodes of depression, and this chronicity increases the risk that they will become disabled.  The SSRIs, to a certain extent, act like a trap in the same way that neuroleptics do.” (p 169-170)

So, since at least 1994 – twenty years ago – researchers and commentators have been adducing evidence and arguments that antidepressants, even though they may have been initially successful in altering feelings of depression, when taken for extended periods may actually lead to persistent, treatment-resistant depression.  Discontinuation of the drug sometimes produces a slow and gradual lightening of the mood, but in some cases this does not occur, and the chronic depression can become more or less permanent.

Amazingly, or perhaps I should say predictably, organized psychiatry has not launched a major investigation into this matter, and I can find no indication that any such investigation is in the works.

In fact, the current (2010) APA treatment guidelines for major depressive disorder state:

“During the maintenance phase, an antidepressant medication that produced symptom remission during the acute phase and maintained remission during the continuation phase should be continued at a full therapeutic dose.” [Emphasis added]

Of course, the APA’s guideline will generate more drug sales.  But surely that wouldn’t be a consideration.  Would it?

SSRIs and Persistent Pulmonary Hypertension of the Newborn (PPHN)

There’s a new study in the January 2014 issue of the BMJ:  Grigoriadis et al, Prenatal exposure to antidepressants and persistent pulmonary hypertension of the newborn: systematic review and meta-analysisThanks to Nanu Grewal for the link.

PPHN is a relatively rare condition.  The authors report that the estimated prevalence is about 1.9 per 1000 live births.  The disease is essentially a failure of the newborn’s circulatory system to switch from oxygen supply via the placental blood, to oxygen supply via the baby’s own lungs.  The condition is usually diagnosed at birth or shortly thereafter.  Symptoms include:  rapid and difficult breathing, fast heart rate, and blue skin color.  PPHN is a serious condition.  A 2010 article by Robin Steinhorn, MD, states:

“Even with appropriate therapy, the mortality for PPHN remains between 5-10%.  In addition, approximately 25% of infants with moderate or severe PPHN will exhibit significant neurodevelopmental impairment at 12-24 months.”

Delaney et al (2012) describe PPHN as “…a syndrome without either optimally effective preventative or treatment strategies,” and states that it “…remains a major cause of morbidity and mortality in neonatal centers across the globe.”

The BMJ article is a meta-analysis, combining the data from seven previous studies that examined the link between maternal use of SSRI’s and PPHN.  Here are their results:


SSRI Use Odds Ratio Confidence Interval 95% Statistical Significance
Early pregnancy 1.23 0.58-2.60 NS
Any time in pregnancy 1.55 0.79-3.04 NS
Most or all of pregnancy 3.33 1.58-7.02 S (0.002)
Late pregnancy 2.50 1.32-4.73 S (0.005)


Essentially what this means is that a woman who used SSRI’s for “most or all” of her pregnancy had a 3.33 times greater risk of delivering a child with PPHN than a woman who had not used SSRI’s.  The risk for late pregnancy use was 2.50 times greater.

Given a baseline prevalence estimate of 1.9 per 1000 births, and an odds ratio of 2.5, the expected incidence of PPHN in late-pregnancy SSRI cases would be about 4.75 (2.5 x 1.9).  This represents an excess of 2.85 cases per 1000 as compared to the general prevalence.


In the article’s abstract, the authors concluded:

“The risk of persistent pulmonary hypertension of the newborn seems to be increased for infants exposed to SSRIs in late pregnancy, independent of the potential moderator variables examined.  A significant relation for exposure to SSRIs in early pregnancy was not evident.”

In the text of the article a more detailed analysis was offered:

“Depression during pregnancy must not be left untreated, as the potential for untoward effects is not negligible and can extend into the postpartum period. Selection of treatment is based on several factors, and antidepressant drugs may be necessary, especially in severe depressive episodes…Although the odds for persistent pulmonary hypertension of the newborn seem to be greater with the use of SSRIs later in pregnancy, despite the limitations of the original studies, the risk is still low. Results from this meta-analysis still concur with earlier statements…that fewer than about 1 infant in 100 will develop persistent pulmonary hypertension of the newborn after antenatal exposure to SSRIs. Although this condition is serious and death rates between 5% and 10% have been reported, when it is associated with other conditions (such as some congenital malformations, meconium aspiration, sepsis, and idiopathic disease), it can be managed favourably…The death rate in infants with persistent pulmonary hypertension of the newborn who have been exposed to SSRIs, however, remains unknown (although one study did report 9.1% of the infants died who were exposed to SSRIs compared with 9.5% of those who were not exposed…”

The deference to the “need” for antidepressant drugs is noteworthy.  This kind of disclaimer has become almost routine in research of this kind.

In my view the essential point of the article is that it demonstrates one more serious adverse effect of these drugs.