Tag Archives: suicide

Neuroleptic Drugs, Akathisia, and Suicide and Violence

Thirty-three years ago, in August 1983, an article titled Suicide Associated with Akathisia and Depot Fluphenazine Treatment appeared in the Journal of Clinical Psychopharmacology.  The authors were Katherine Shear, MD, Allen Frances, MD, and Peter Weiden, MD.

Here are some quotes, interspersed with my comments/observations:

“Akathisia is a common and distressing side effect of neuroleptic medication that can be difficult to recognize and treat.  Several previous reports mention maladaptive behavioral consequences, such as poor compliance with prescribed medication and aggressive or self-destructive outbursts.  We are reporting suicides in two young Hispanic men who had developed severe akathisia after treatment with depot fluphenazine.  Depression with suicidal behavior has been observed following fluphenazine injection, but suicide associated with akathisia has not been previously noted.”

Fluphenazine is a neuroleptic drug of the phenothiazine class that was introduced in 1959.  It is marketed as Prolixin and other brand names, and according to Wikipedia, is on the WHO’s “List of Essential Medicines, most important medications needed in a basic health system.”

The “treatment” used in each case was a depot injection of fluphenazine.  This is a long-lasting injection, typically 30 days, in which the drug is lodged in a dermal or muscular mass from which it is slowly drawn into the blood stream.  (Hence depot:  a place where goods are stored for later distribution.)

Depot injections have some obvious convenience value, but in psychiatry are usually used to ensure compliance.  Their major downside is that if the person has an adverse reaction to the drug, there’s no way to remove the stored chemicals from his body.

The authors may be correct in stating that this is the first published report of suicide associated with akathisia, but it is not the first report of suicide associated with fluphenazine.  Seventeen years earlier, Dorothy West, MD, had published the following letter in the British Journal of Psychiatry, 117 (1970), 718-9.


Dear Sir,

A new drug is being widely used in the treatment of mental illness.  It is long-acting and used by injection – its name is fluphenazine (Moditen).  Is this the thalidomide of the 70’s?  I would like to have the opinion of other doctors.  Whilst it is still new maybe we are lulled into a false sense of security, but are we justified in using a drug, which may take up to six weeks to eradicate from the tissues, without being sure of its safety?  Its side effects alone are legion.  A study of 13 papers gives the following:
Common side-effects reported are – lethargy, drowsiness, dizziness, muscular inco-ordination, paraesthesia, hypotension, blurring of vision, dryness of mouth, malaise, feelings of tension, confusion, nausea, vomiting, and aches and pains.
Parkinsonism is extremely common.  Incidence in reports varies from 100 per cent to 24 per cent with many reports around 50 per cent.
Depression is quite common and tends to be severe – 5 suicides reported and two suicide attempts.
Other reported side-effects include psychotic relapse and glaucoma.

Dorothy West”

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

Back to the Shear, Frances, and Weiden paper:

Case Reports

“Case 1

A 23-year-old single unemployed Hispanic man had been socially withdrawn, blunted in affect, and thought disordered since his early teenage years.  He was intermittently delusional with auditory hallucinations which responded to phenothiazines.  He was treated in a day hospital after one of multiple hospitalizations; depot fluphenazine was used because of medication noncompliance.  He received two injections of 25 mg of fluphenazine decanoate separated by 1 week, with noticeable improvement in his psychotic symptoms.  He also developed akathisia and was prescribed trihexyphenadyl, 2 mg twice a day, which he probably did not take.  There was no improvement in his akathisia and no anticholinergic side effects.  He soon stopped attending the day hospital and a family member called a week later to say that the man had killed himself by jumping off the roof of their building.  He had given no indication of being suicidal and his family believed the increased ‘nervousness’ had driven him to this desperate measure.  The patient had no previous history of suicidal behavior and did not drink alcohol or use drugs.”

So, we have a young man who has been socially withdrawn and joyless since his early teens.  Not surprisingly his perceptions and thinking patterns deviated from the conventional.  For reasons unknown he came within the orbit of psychiatry, and had had extensive contact with the psychiatric system.  He was given two depot injections of fluphenazine one week apart.  His “psychotic symptoms” improved, but he developed akathisia.  He was prescribed an anticholinergic agent to combat the akathisia, but apparently this was ineffective, or as the authors suggest, he didn’t take it.  In any event, a week later he killed himself by jumping from the roof of a building.

We don’t know if the fluphenazine was administered involuntarily, but we do know that he had taken phenothiazine in the past and had been noncompliant.  So it is reasonable to assume that there was some adverse effect.  Did the day hospital psychiatrists explore the reason for this “noncompliance”?  In any event, given the outcome, the phrase “depot fluphenazine was used because of medication noncompliance” is a haunting and compelling testament to psychiatric arrogance.  This anonymous young man was clearly prone to acute akathisia, and his “noncompliance” was a sensible and correct response to the neuro-poisoning he was receiving from psychiatrists.  He stopped attending the day hospital (again, understandably),but he had no way to get the drug out of his body.  The trihexyphenidyl is an anticholinergic agent and might have mitigated the akathisia.  Or perhaps he took it and it was not effective, as is frequently the case.

“Case 2

A 36-year-old non-English speaking Hispanic man was seen once in our walk-in clinic because of severe restlessness and leg cramps.  Intermittent somatic symptoms and nervousness began shortly after he arrived in the United States 8 months earlier.  When the symptoms worsened, he began a series of visits to hospital emergency rooms and private psychiatrists.  Three weeks before the walk-in visit a Spanish-speaking psychiatrist diagnosed paranoid schizophrenia and administered depot fluphenazine.  Following this injection, the patient developed a dystonic reaction and then began to complain continuously of leg cramps and restlessness.  In the ensuing weeks he received numerous drugs from emergency room or private physicians, some given by injection and some by prescription.  He brought bottles of thiothixene, chlorazepate, amitriptyline, meprobamate, and lorazepam to the clinic.  He was agitated, paced, and begged for help.  He denied symptoms of depression or suicidal ideation.  He claimed he was devoted to his wife and 9-year-old daughter, but he felt his unbearable symptoms would never go away.  He made good contact in a translated interview and showed no thought disorder, hallucinations, or delusions.  Thorough medical examination was negative except for the parkinsonian symptoms.  He had no prior history of psychiatric treatment and the family history was negative for depression, nervousness, and significant psychiatric or medical illness.  Since the diagnosis was uncertain, plans were made to discontinue all medication and a follow-up appointment was scheduled.  The next day he killed himself without warning by jumping in front of a subway train.”

The 36-year-old man had come to the US eight months earlier, and had begun to experience “somatic symptoms and nervousness”.  This seems hardly surprising in someone who is having to adapt to a new environment, but we are provided no details with regards to his psychosocial context, other than the fact that he had a wife and 9-year-old daughter, and that he didn’t speak English.  What we do know is that he visited “emergency rooms and private psychiatrists” to help with “somatic symptoms and nervousness”.  One of the psychiatrists “diagnosed paranoid schizophrenia”, and gave him a depot injection of fluphenazine.  He developed severe akathisia, and continued to visit emergency rooms and private psychiatrists in an attempt to gain some relief.  During this period he received “numerous drugs” from these sources, some by injection, some by prescription.  At this point he came to the authors’ walk-in clinic.

“He was agitated, paced, and begged for help.”


“He denied symptoms of depression or suicidal ideation.  He claimed he was devoted to his wife and 9-year-old daughter, but he felt his unbearable symptoms would never go away.”

Plans were made to discontinue all the drugs, which the authors euphemistically refer to as medications, but it was too little, too late.  He jumped to his death in front of a train the next day.

So, we have a healthy young man, devoted to his wife and daughter, who seeks medical help for what were probably stress-related “somatic complaints and nervousness”.  Psychiatrists throw a bewildering array of drugs at him, including a depot injection of fluphenazine, which results in his death.  And the only reason we know about this forgotten victim of psychiatry is because the authors wrote up and published the case.  How many other thousands have died from the same kind of irresponsible drug-pushing; from the same arrogant conviction that for every human problem, psychiatry has a “safe and effective” pill?

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

Here are some more quotes from the Shear et al article:

“Akathisia is an intensely unpleasant feeling characterized by muscle discomfort, inability to sit still, continuous agitation, restlessness, and fidgety feelings.  Sleep may be disturbed by an inability to lie down.  Some patients say they feel like jumping out of their skin”

“The estimated incidence of akathisia with neuroleptic use ranges from 20 to 45%.  Several studies using depot fluphenazine report an incidence around 35%.”

“Akathisia is a distressing  symptom which may be difficult to diagnose and treat.  Restlessness may be mistaken for anxiety and clinicians may err by raising neuroleptic dosage.”

“Sometimes the only effective treatment is withdrawal of the neuroleptic.  Although we cannot be sure that akathisia caused the deaths of our patients, akathitic symptoms seemed to be immediate precipitants of suicidal behavior.   We urge clinicians to be alert to the discomfort of akathisia and to treat it aggressively.  If treatment with anticholinergics or γ-aminobutyric acid agonists fails or symptoms are especially severe, hospitalization may be indicated.”

It is clear that the authors are leaning heavily towards the conclusion that neuroleptic-induced akathisia was the immediate precipitant of both suicides.


Several similar reports have appeared in the literature for decades.  Here are some examples, with relevant quotes:

Van Putten, T., MD, The Many Faces of Akathisia, Comprehensive Psychiatry, 1975, 16(1):

“AKATHISIA, a common side effect of neuroleptic therapy, is an emotional state and ‘refers not to any type or pattern of movement, but rather to a subjective need or desire to move.'”

“A 44-year-old woman with hebephrenic schizophrenia started to bang her head against the wall three days after an injection of 25 mg of fluphenazine enanthate.  Her only utterance was: ‘I just want to get rid of this whole body.'”

“Akathisia is often associated with strong affects of fright, terror, anger or rage, anxiety, and vague somatic complaints.”

“On this regime, she usually developed an episode of akathisia during the week following her injection.  She described several such episodes as follows: ‘I just get these attacks of tension.  I don’t feel right.  My stomach feels strange.  It’s like I’m churning inside.  I feel hostile and I hate (with intense affect) everybody.”

“Patients have described the inner restlessness and agitation of akathisia in many other ways, such as:  ‘My nerves are just jumping’ I feel like I’m wired to the ceiling; I just feel impatient and nasty.  I can’t concentrate; it’s like I got ants in my pants; my nerves are raw; I just feel on edge; I feel just nasty; I feel like jumping out of my skin; if this feeling continues, I would rather be dead.  I can’t describe the feelings; I’m quivery from the waist up; I want to climb the walls; I feel all revved up; it’s like I got diaper rash inside.'”

“Patients with severe akathisia, however, cannot sit quietly for more than a few seconds at a time, and at times the ‘impatience musculaire’ can result in running, agitated dancing, or rocking.”

“Akathisia is tolerated very poorly by hostile paranoid patients in that they tend to misinterpret the inner agitation of akathisia as further proof that they are being poisoned or controlled by outside malevolent forces.”

Note the presumably unintended irony in the word misinterpret.  In reality, they are being poisoned and controlled by outside forces!

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

Keckich, W., MD:  Neuroleptics: Violence as a Manifestation of Akathisia, JAMA, 1978, Nov 10 (240) 20, 2185:

“NEUROLEPTIC medications (eg, phenothiazines, butyrophenones) are used in medicine to control psychotic symptoms and concomitant agitated and violent behavior. They also are used to control anxiety and agitation whenever minor tranquilizers (eg, benzodiazepines) would be inappropriate. Development of akathisia as a parkinsonian side effect is confirmed in the use of these drugs.  Akathisia is a condition that gives rise to the subjective desire to be in constant motion, with a feeling of inner agitation and muscle tension. The patient cannot sit still and paces constantly”

“One week later the patient reported that he was more agitated at night.  Since it was not known at the time that akathisia was beginning, haloperidol treatment was increased to 4 mg at bedtime to decrease the agitation. Four days later, after his evening dose of 4 mg of haloperidol, he became uncontrollably agitated, could not sit still, and paced for several hours.  He complained of tightness in his muscles, rigidity, a jumpy feeling inside, and violent urges to assault anyone near him.  This culminated in an assault on his dog with an intent to kill.  He became frightened over his loss of control and came to the emergency room.  He was given 50 mg of thioridazine hydrochloride, which brought the hostility under control but did not remove it.

He subsequently discontinued the treatment with imipramine and haloperidol.  The following morning he reported that the muscle tightness, jumpy feelings, and hostility were decreased but still present.  Three days after drug treatment was discontinued all of the symptoms had ceased, and he was at his baseline of difficulty once again.  The half-life of haloperidol is approximately 24 hours, and this symptom relief coincided with expected excretion of the drug.

In retrospect it was apparent that he had experienced increasing akathitic side effects from the haloperidol medication, which accounted for his increasing night-time agitation and culminated in a stimulation of violent and aggressive activity.”

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

Schulte, JL, MD, Homicide and Suicide Associated with Akathisia and Haloperidol, American Journal of Forensic Psychiatry, Jan 1985, 6(2):

“The following five cases are reported to bring attention to the potential for severe violence, as a result of akathisia, following such administration of a neuroleptic for acute psychiatric symptoms.  Particular emphasis is directed to an experience of sensory dissociation associated with the uncomfortable physical reactions, resulting in extreme acts of physical violence.”


“A 23-year-old married, Salvadorian-born male, with a four-day history of progressive paranoia and disorganized behavior, had been taken by the police department to a hospital at the request of his parents.  The physician insisted he receive an injection of haloperidol in the emergency room while awaiting admission to the psychiatric unit where he had previously been a patient on a number of occasions.

  He tried to resist but felt he had no option with the staff and police surrounding him.  He felt he was being unnecessarily delayed in being admitted to the inpatient unit.  In addition, he felt he had been lied to, in that apparently he had been told he was going to see his wife who had deserted him approximately 48 hours earlier.  He then escaped from the emergency room and the authorities, ran several miles to a park, tried to get a policeman to help him, escaped again and totally disrobed.  Within the next 45-minute period of time, he assaulted one woman who was walking her dog and attempted to rape her.  When pulled off by the husband, he proceeded down the street, broke down the front door of a house where an 81-year-old lady was sleeping.  He severely beat her with his fists, ‘to a pulp’, by his own description.  Following which he found knives and stabbed her repeatedly, resulting in her death.  Then, after being confronted in the street by a policeman who sprayed him with Mace, he returned through the house, exiting the back door where he ran into another woman with her child.  He repeatedly stabbed the woman in front of the child, whereupon he moved on to the next person he encountered, a woman whom he severely assaulted and stabbed to the extent that an eye was lost and an opening into the anus was created resulting in major surgery and serious residual problems, including a colostomy.  He was then finally captured and subdued by eight policemen and hospitalized.

He had ten previous psychiatric hospitalizations between 1975 and the present.  All of these hospitalizations have been only a matter of hours to several days.  He would always be placed on medication and released, following which he would stop taking the medication and go along until another upheaval would occur.

He had a history of problems with anger and acute paranoid beliefs leading to hyperactive behavior and one incident in which it was reported he tried to choke one of his brothers.

His description of his mental status at the time of his offense is quite striking.  He describes himself as feeling almost like a spectator in a movie.  He makes a point of describing how he had lost all sense of caring about anything or anyone in life.  Additionally, he describes a feeling of loss of physical sensation, including feeling nothing when maced by the police.  He felt enormous energy with a feeling of needing to rid himself of it.

He gives the history of having been picked up by the police on a traffic violation in 1979 and placed in jail for the first time in his life.  He became angry and was given a series of haloperidol injections, becoming progressively more agitated and unmanageable to the point he was rolled up in a mattress and handcuffed in order to be transported to a psychiatric inpatient unit.  In 1980, during another hospitalization, he was, despite his protests, changed from chlorpromazine to haloperidol and within hours became totally unmanageable, requiring six individuals to subdue him and place him in seclusion and restraint.” [Emphasis added]

It is noteworthy that this individual asked not to be changed from chlorpromazine to haloperidol, but his request was ignored.

Eight years later, Herrera et al confirmed in a controlled study that an increase in violent behavior was more likely with haloperidol than with chlorpromazine.  Apparently, the individual had some intuitive awareness of this from previous experience, but as is often the case, the psychiatrists discounted his protests and gave him the haloperidol anyway.

Here are two quotes from the Herrera et al study:

“We found in a controlled study that some patients have a marked increase in violence when treated with moderately high-dose haloperidol.”

“…these patients did not show an increase in violence during a placebo period, nor did they have a history of violent behavior.”

Back to the Schulte JL article:


“A 30-year-old man with a history of mental illness dating back seven years, with hospitalizations in three other states, was admitted to the hospital on six counts of burglary. His diagnosis was paranoid schizophrenia, and he had been found not guilty by reason of insanity by the courts. The admission note by the psychiatrist stated, ‘He is somewhat paranoid, but says he has side effects from most tranquilizers.’ On the third day of hospitalization, he was referred to the psychiatrist by nurses because of difficulty getting to sleep. No evidence of aggressiveness or self-injurious behavior was charted that day in the nurses’ notes.  The psychiatrist prescribed haloperidol, 5mg. three times a day, which was begun the next day, with three doses administered with Cogentin, 2mg twice a day. Nurses’ notes that day stated, ‘He was very anxious about being in the hospital and threatened to kill himself if he gets up the nerve.’ At 10:45 p.m., notes stated, ‘He has regressed during this shift in all assessment areas. His hygiene is poor, and he is irresponsible, e.g., lying on the floor without shoes or socks.’  He refused medication initially at 5 p. m., and stated that phenothiazines, ‘fuck me up.’  He finally took the medication but then stated angrily, ‘Now I’ll  really get crazy.’  He ranted loudly and profanely for 30 minutes. He took his 9 p.m. medication and started his haranguing again, only louder and more threatening. ‘l’ll kill all of you mother-fuckers before I leave here,’  He was found in his room at 6:50 a.m., having hung himself with a bed sheet. A letter from his attorney to the hospital had stated that ‘medications caused him problems (l should perhaps state that by medications I mean psychotropic drugs).'” [Emphasis added]


“A 52-year-old male first came to psychiatric attention eleven years earlier following an assault on his wife. He had delusions of cancer, a belief he would die and felt sexually inadequate.

He had been unsuccessfully treated with Lithium and antidepressants, as well as various tranquilizers. He had continually been an inpatient or in board and care facilities, and three and one-half months earlier, he had his medications changed to 10mg. of Haloperidol in the a.m. and 40mg. of Haloperidol at hour of sleep, with 2mg.of Artane twice daily. Each month he stated he complained to his psychiatrist of severe restlessness. He stated he had to roll over and over in bed at night and usually would be unable to get to sleep until 3 or 4 a.m. During the day, he would try to lie down but couldn’t because of his severe uncomfortableness. He described after being turned down again by the psychiatrist, he became despondent and angry, lost hope and decided if he could not ever even sleep like the rest of his boarding home mates that life wasn’t worthwhile.  He secured a knife and repeatedly stabbed himself in the abdomen, was rushed to the hospital and barely survived.  He remarked he could never even feel the knife when stabbing himself.” [Emphasis added]

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

Van Putten, T. MD and Marder, SR, MD, Behavioral Toxicity of Antipsychotic Drugs, J Clin Psychiatry, September 1987, 48: 9 (Suppl):

“The subjective restlessness of akathisia is usually accompanied by telltale foot movements: rocking from foot to foot while standing or walking on the spot. Akathisia is strongly associated with depression and dysphoric responses to neuroleptics and has even been linked to suicidal and homicidal behavior in extreme cases.”

“The aforementioned case literature reads convincingly:  it is reasonable to conclude that akathisia, in the extreme case, can drive people to suicide or homicide.”

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

Crowner, ML, Douyon, R, et al, Akathisia and violence Psychopharmacology Bulletin, 1990: 26(1): 115-7:

“Akathisia is a common side effect of neuroleptic drugs that may present with behavioral disturbances. There have been preliminary reports on the association between violence and akathisia. We report the first observational study of this relationship. Patients studied were from a special unit for violent patients. A closed-circuit television camera was installed in each of the corners in its dayroom. Incidents of assault plus the 5 minutes preceding each assault were recorded on videotape. Participants and bystanders were rated for the motor component of akathisia. For each of nine incidents, we compared the akathisia scores for participants and for bystanders. Both victims and assailants were akathisic before about half of all incidents; bystanders rarely were. The classification of the movements we rated and the implications for further studies are discussed.”

The extraordinary irony here is that the individuals in this study “were from a special unit for violent patients,” but in fact the drug used to control this behavior was actually precipitating more violence!

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

Galynker, I, MD, PhD and Nazarian, D, MD, letter to the editor, Journal of Clinical Psychiatry, 1997, 58: 31-32:

“Case ReportMr. A, a 47-year-old white man with a diagnosis of bipolar mood disorder, was brought to the emergency room because he was screaming in the streets.  Mr. A had over 30 past psychiatric admissions associated with agitation and violence and was often discharged against medical advice.  He was nearly always noncompliant with his antipsychotic medications, claiming that they made him ‘jump and lose my temper.’  Prior to the present admission, Mr. A’s daily medications included haloperidol 20 mg, lithium carbonate 1500 mg, divalproex sodium 500 mg, and benztropine 1 mg.  At admission, the patient was grandiose, had loud and pressured speech, and admitted he was not taking haloperidol.  He was given haloperidol 15 mg q.h.s. and benztropine 1 mg q.a.m.  Within 24 hours he started pacing; became restless, agitated, and violent; complained of feeling ‘jumpy’; and attacked a staff member.  On Day 5 of his hospitalization, haloperidol and benztropine were discontinued; chlorpromazine was started, and the dose was increased to 950 mg/day.  Mr. A, although sedated, remained threatening and violent.  On Day 13, chlorpromazine was discontinued, and haloperidol was restarted at a higher dose of 15 mg p.o. b.i.d.  Mr. A again complained of ‘jumpiness’ and punched a television cabinet, causing a self-inflicted fracture.  On hospital Day 17, owing to an error, haloperidol was discontinued.  The patient became calmer, less irritable, displayed no angry outbursts, and required no further room restrictions.  After 5 days, when the error was discovered, haloperidol was restarted at a lower daily dose of 10 mg.  Within 3 days, the patient became violent and required room restriction.  Haloperidol was then discontinued, the patient’s agitation and violence resolved, and a week later he was discharged.  His daily medications were lithium carbonate 1500 mg (serum level = 0.9mEq/L; this dose had not been changed during his hospitalization), lorazepam 1 mg, and divalproex sodium 500 mg.  On these mediations, he remained well 6 months postdischarge, his longest period as an outpatient.”

In their commentary, the authors point out:

“The fact that the jumpiness occurred with haloperidol and not with chlorpromazine is another factor indicative that Mr. A has exhibited akathisia rather than nonspecific activation of mania; this is because akathisia is more common with higher potency as compared with low-potency neuroleptics.”

and, with more candor than one customarily finds in psychiatry:

“One can also speculate that Mr. A’s rocky clinical history was related to aggressive behavior perpetuated by antipsychotic administration.”

And it is worth remembering that Mr. A’s “rocky clinical history” entailed “over 30 past psychiatric admissions associated with agitation and violence”.

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

So, since at least the early 80’s, individual psychiatrists have been drawing attention to the fact that neuroleptic drugs induce akathisia in many cases, and that in some cases this can precipitate suicide and/or homicide.


Although it is well known that neuroleptic drugs cause akathisia, the link between antidepressants and this condition is less widely appreciated.  The Wikipedia article on akathisia contains this:

“Antidepressants can also induce the appearance of akathisia, due to increased serotonin signalling within the CNS.”

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

Hamilton, MS, MD, Obler, LA, Akathisia, suicidality, and fluoxetine, J Clin Psychiatry, 1992, Nov 53(11), 401-406, write:

“The propose[d] link between fluoxetine and suicidal ideation is explained by fluoxetine-induced akathisia and other dysphoric extrapyramidal reactions.”


“The literature suggests that fluoxetine-induced extrapyramidal reactions may be a mediator of de novo suicidal ideation.”

Fluoxetine is an SSRI, marketed as Prozac, Sarafem, and other names.

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

Wirshing, WC, MD, Van Putten, T, MD, Rosenberg, J, MD, et al, Fluoxetine, Akathisia, and Suicidality: Is There a Causal Connection?, Arch Gen Psychiatry, 1992, 49(7), 580-581, write:

“We have now had experience with five such patients.  All were women.  None had a history of significant suicidal behavior; all described their distress as an intense and novel somatic-emotional state; all reported an urge to pace that paralleled the intensity of the distress; all experienced suicidal thoughts at the peak of their restless agitation; and all experienced a remission of their agitation, restlessness, pacing urge, and suicidality after the fluoxetine was discontinued. We describe herein five cases of what we think might be fluoxetine-induced akathisia accounting for suicidal ideation.”

Eikelenboom-Schieveld, SJM, Lucire, Y, MD, Fogleman, J, PhD, The relevance of cytochrome P450 polymorphism in forensic medicine and akathisia-related violence and suicide, Journal of Forensic and legal Medicine, 2016, 41. 65-71, wrote:

“Antidepressants have been reported as causing suicide and homicide and share the class attribute of frequently producing akathisia, a state of severe restlessness associated with thoughts of death and violence.”


“In this paper, we report our investigation into adverse drug reactions/interactions in three persons who committed homicide, two also intending suicide, while on antidepressants prescribed for stressful life events”


“Three persons committed homicide, two of which intended to commit suicide. None had been aggressive or mentally ill before getting medication. None had known that they needed to take medication regularly or how to stop taking it safely. None improved on medication, and no prescriber recognized their complaints as adverse drug reactions or was aware of impending danger. Interviews elicited accounts of restlessness, akathisia, confusion, delirium, euphoria, extreme anxiety, obsessive preoccupation with aggression, and incomplete recall of events. Weird impulses to kill were acted on without warning. On recovery, all recognized their actions to be out of character, and their beliefs and behaviours horrified them.”

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

Whitehead, PD, Causality and Collateral Estoppel: Process and Content of Recent SSRI Litigation, 2003, J Am Acad Psychiatry Law 31:377–82, wrote:

“In Tobin v. SmithKline Beecham Pharmaceuticals a jury in the U.S. District Court for the District of Wyoming found that the medication Paxil ‘can cause some individuals to commit homicide and/or suicide,’ and that it was a legal cause of the deaths in this case.”

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

Breggin, PR, MD, Suicidality, violence and mania caused by selective serotonin reuptake inhibitors (SSRIs): A review and analysis. International Journal of Risk & Safety in Medicine, 2004, 16, 31-49, wrote:

“Evidence from many sources confirms that selective serotonin reuptake inhibitors (SSRIs) commonly cause or exacerbate a wide range of abnormal mental and behavioral conditions. These adverse drug reactions include the following overlapping clinical phenomena: a stimulant profile that ranges from mild agitation to manic psychoses, agitated depression, obsessive preoccupations that are alien or uncharacteristic of the individual, and akathisia. Each of these reactions can worsen the individual’s mental condition and can result in suicidality, violence, and other forms of extreme abnormal behavior.  Evidence for these reactions is found in clinical reports, controlled clinical trials, and epidemiological studies in children and adults. Recognition of these adverse drug reactions and withdrawal from the offending drugs can prevent misdiagnosis and the worsening of potentially severe iatrogenic disorders. These findings also have forensic application in criminal, malpractice, and product liability cases.”


“There are many reports and studies confirming that SSRI antidepressants can cause violence, suicide, mania and other forms of psychotic and bizarre behavior.”

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

Although there is a great deal of prima facie evidence and many case reports detailing the neuroleptic/antidepressant link to suicide and violence, there has not to my knowledge been a definitive large-scale study by American psychiatry of the link between psychiatric drugs and the murder/suicides that are occurring with increased frequency.

And the great question is:  why not?  Why is this urgent, life-threatening issue not afforded the highest priority by the APA, NIMH, and university psychiatry departments?  Is their self-serving need to protect psychiatry from the consequences of its errors eclipsing their ethical integrity and their sense of responsibility?


In this regard, it’s interesting to see how psychiatric drug-induced akathisia has been handled in the various editions of DSM.

DSM-III-R (1987) makes no specific reference to neuroleptic or antidepressant-induced akathisia.  There are, however, a number of statements in the chapter on “schizophrenia” which clearly (and deceptively) ascribe symptoms of akathisia and tardive dyskinesia to “schizophrenia” itself.  For instance:

“In addition, odd mannerisms, grimacing, or waxy flexibility may be present [in schizophrenia]. (p 190)

“Almost any symptom can occur as an associated feature [of schizophrenia].  The person may appear perplexed, disheveled, or eccentrically groomed or dressed. Abnormalities of psychomotor activity—e.g., pacing, rocking, or apathetic immobility—are common.” (p 190) [Emphasis added]

In reality, most of the pacing, grimacing, and rocking exhibited by people labeled schizophrenic is a direct result of neuroleptic drug poisoning, and not an associated feature of the so-called illness itself.

“Dysphoric mood is common [with schizophrenia], and may take the form of depression, anxiety, anger, or a mixture of these.” (p 190)

Anxiety and anger are also direct effects of neuroleptic poisoning for many people.

“Although violent acts performed by people with this disorder often attract public attention, whether their frequency is actually greater  than in the general population is not known.  What is known is that the life expectancy of people with Schizophrenia is shorter than that of the general population because of an increased suicide rate and death from a variety of other causes.” (p 191)

As is clear from the material quoted earlier, suicide is frequently a result of akathisia.  The phrase “death from a variety of other causes” is unclear.

. . . . . . . . . . . . . . . . 

DSM-IV (1994) was markedly more honest in acknowledging the existence of neuroleptic-induced akathisia.  In fact, this was included as an actual diagnosis in the fourth edition.  It was coded as 333.99, and 2½ pages (744-746) were devoted to its description.  Here are some quotes:

“In its most severe form, the individual may be unable to maintain any position for more than a few seconds.” (p 744)

“The subjective distress resulting from akathisia is significant and can lead to noncompliance with neuroleptic treatment.  Akathisia may be associated with dysphoria, irritability, aggression, or suicide attempts.  Worsening of psychotic symptoms or behavioral dyscontrol may lead to an increase in neuroleptic medication dose, which may exacerbate the problem.  Akathisia can develop very rapidly after initiating or increasing neuroleptic medication.  The development of akathisia appears to be dose dependent and to be more frequently associated with particular neuroleptic medications.  Acute akathisia tends to persist for as long as neuroleptic medications are continued, although the intensity may fluctuate over time.  The reported prevalence of akathisia among individuals receiving neuroleptic medication has varied widely (20%-75%).” (p 745) [Emphasis added]

Note the reference in the third line above to “irritability, aggression, or suicide attempts“.  In fact, as the material quoted earlier makes clear, neuroleptic-induced akathisia has been causally-linked to actual homicides and suicides.  This understatement was clearly deliberate, as Allen Frances, MD, architect of DSM-IV, was also one of the authors of the Shear et al paper quoted earlier, which linked neuroleptic-induced akathisia to actual completed suicides.

“Neuroleptic-Induced Acute Akathisia may be clinically indistinguishable from syndromes of restlessness due to certain neurological or other general medical conditions, to nonneuroleptic substances, and to agitation presenting as part of a mental disorder (e.g., a Manic Episode).” (p 745)

In other words, people who are experiencing neuroleptic-induced acute akathisia are at risk of being assigned a “diagnosis” of “bipolar disorder”!

Serotonin-specific reuptake inhibitor antidepressant medications may produce  akathisia that appears to be identical in phenomenology and treatment response to Neuroleptic-Induced Acute Akathisia.  Akathisia due to nonneuroleptic medication can be diagnosed as Medication-Induced Movement Disorder Not Otherwise Specified.” (p 745) [Bold face in original]


“Individuals with Depressive Episodes, Manic Episodes, Generalized Anxiety Disorder, Schizophrenia and other Psychotic Disorders, Attention-Deficit/Hyperactivity Disorder, dementia, delirium, Substance Intoxication, (e.g., with cocaine), or Substance Withdrawal (.e.g., from an opioid) may also display agitation that is difficult to distinguish from akathisia.” (p 745-746) [Bold face in original]

Which prompts one to wonder how many people who have been assigned these so-called diagnoses were actually suffering from one of the toxic effects of neuroleptic drugs or SSRI’s.  It is also entirely plausible, as DSM-IV suggests, that many of these individuals would have been “treated” with even higher doses of neuroleptics!

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

The entry in DSM-IV-TR (2000) is identical to that in DSM-IV except for the following addition:

“Although the atypical [newer] neuroleptic medications are less likely to cause akathisia than the typical [older] neuroleptics, nonetheless, these medications do cause akathisia in some individuals.” (p 801)

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

DSM-5 is remarkably less frank concerning psychiatric drug-induced akathisia than was DSM-IV.  The name Neuroleptic-Induced Acute Akathisia was changed to Medication-Induced Acute Akathisia and the entry is given a total of four-and-a-half lines of text:

333.99 (G25.71)  Medication-Induced Acute Akathisia
Subjective complaints of restlessness, often accompanied by observed excessive movements (e.g., fidgety movements of the legs, rocking from foot to foot, pacing, inability to sit or stand still), developing within a few weeks of starting or raising the dosage of a medication (such as a neuroleptic) or after reducing the dosage of a medication used to treat extrapyramidal symptoms.” (p 711) [Bold face in original]

There is no reference to the fact that, as earlier psychiatric authors had stated, the condition can be so unbearable as to drive people to suicide and even homicide.

There is, however, an interesting admission in a separate, also brief, entry:

“333.72 (G24.09)  Tardive Dystonia
 333.99  (G25.71)  Tardive Akathisia
Tardive syndrome involving other types of movement problems, such as dystonia or akathisia, which are distinguished by their late emergence in the course of treatment and their potential persistence for months to years, even in the face of neuroleptic discontinuation or dosage reduction.” (p 712) [Bold face in original]

In other words, neuroleptic-induced akathisia can persist for years, even if the person stops taking the drugs!  But even granting this admission, it is clear that DSM-5 is markedly down-playing the significance and seriousness of neuroleptic-induced akathisia.  And it is also clear from elsewhere in the text that the agenda here is to protect the reputation of the neuroleptic drugs:

“The term neuroleptic is becoming outdated because it highlights the propensity of antipsychotic medications to cause abnormal movements, and it is being replaced with the term antipsychotic in many contexts.” (p 709)

Note the deceptive use of the passive voice (“is becoming outdated”).  In reality, psychiatrists are consciously and deliberately phasing out the term “neuroleptic” in an attempt to conceal, or at least not draw attention to, the severe and potentially life-threatening neurotoxic effects of these drugs.

But the more important question is why has the APA eliminated the DSM-IV category “neuroleptic-induced akathisia” that ran to 2 ½ pages, and replaced it with the more general “medication-induced acute akathisia”, which runs to 4 ½ lines?  Why has this dangerous and relatively widespread adverse effect been so downplayed?  On page 809 of the DSM-5 text there is a section called Highlights of Changes from DSM-IV to DSM-5, but there is no explanation for the change there.  There is a note in this section referring the reader to “An expanded description of nearly all changes…” on the APA website.  The link leads to an article titled “Highlights of Changes from DSM-IV-TR to DSM-5“.  But the article contains no reference to the change in question.

So we don’t know the APA’s justification for suppressing information about this potentially devastating adverse effect.  But we do know that neuroleptic drugs are being prescribed for an increasing range of problems, and are even being prescribed to toddlers for temper tantrums and to nursing home residents for “management problems”.  Some have even acquired “block-buster” sales status.  It is clearly in pharma’s interests to suppress this information and it is consistent with psychiatry’s hand-in-glove relationship with pharma that they should oblige their generous benefactors in this way.  Remember, 69% of the DSM-5 workforce were in the pay of pharma while working on the revision.

Despite the early, and very clear, statements from individual psychiatrists linking psychiatric drugs to murder/suicides, the psychiatric leadership has consistently failed to address this link.  Instead, they deceptively attribute these incidents to a lack of psychiatric “treatment”, and they call for legal enforcement of even more drugging.


On June 9, 2016, Maria Oquendo, MD, President of the APA, wrote a post in support of the Senate’s so-called Mental Health Reform Bill.  The post was standard psychiatric propaganda, including the inane 21% annual and 50% lifetime prevalence of “mental illness”.  The reality is that if one can invent illnesses at will and arbitrarily reduce the “diagnostic” thresholds of these “illnesses”, one can produce any prevalence numbers one chooses.

The post also drew attention to the fact that there were 41,000 suicides in the US in 2013, and asserted that “…we continue to fail people with mental illness every day.”

In other words, more psychiatric treatment would reduce the suicide rate.  But meanwhile, we have no data on how many of these individuals were in the throes of neuroleptic or antidepressant-induced akathisia.  And as long as psychiatry and pharma are controlling the research agenda, such information will be systematically repressed.

As I’ve stated many times, psychiatry is intellectually and morally bankrupt.  They are adamantly resistant to anything resembling critical self-appraisal, and there are no depths of deception and spin to which they will not go, to suppress the reality and the consequences of their drug-pushing depredations.  Neuroleptic and antidepressant drugs induce some individuals to take their own lives and/or the lives of others.  Neuroleptic and antidepressant drugs are almost certainly the proximate causes of many of the mass shootings that have plagued our country for almost twenty years.  How much longer can psychiatry sustain this dreadful, self-serving deception?


Senator John McCain and Congressman David Jolly have introduced bills in their respective chambers that if enacted will require the Veterans Administration to conduct a comprehensive study of the link between psychiatric drugs and veterans’ suicides.  It will be an enormous step forward if these bills become law.  It is also an interesting reflection that these bills were initiated by politicians, and not by psychiatrists, who present themselves as caring professionals acting in the best interests of their so-called patients.

If you live in the US, please encourage your representatives to support the McCain and Jolly bills (S 3410 and H 4640).

A Bill to Explore the Relationship Between Veteran Suicides and Prescription Medication

On September 28, US Senator John McCain (R-AZ) introduced a bill in the Senate titled Veteran Overmedication Prevention Act (S. 3410).  This is a companion bill to HR 4640, Veteran Suicide Prevention Act introduced in the House by Congressman David Jolly (R-FL) earlier this year.  The objective of both bills is to combat suicide deaths by ensuring that accurate information is available on the relationship between suicides and prescription “medication”.  At the present time, 20 US veterans a day are dying by suicide.

In a September 28 press release, Senator McCain is quoted:

“‘Combatting this [suicide] epidemic will require the best research and understanding about the key causes of veteran suicide, including whether overmedication of drugs, such as opioid pain-killers, is a contributing factor in suicide-related deaths. This legislation would authorize an independent review of veterans who died of suicide or a drug overdose over the last five years to ensure doctors develop safe and effective treatment plans for their veteran patients. We have a long way to go to eradicate veteran suicide, but this legislation builds on important efforts to end the tragedy that continues to claim far too many lives far too soon.'”

Clearly in the press release there is an emphasis on opioid pain-killers, but the problem of psychiatric drugs is also addressed in the bill.  The bill mandates

“…a review of the deaths of all covered veterans who died by suicide during the five-year period ending on the date of the enactment of this Act.”

and the review shall include:

“(E) A comprehensive list of prescribed medications and legal or illegal substances as annotated on toxicology reports of covered veterans described in subparagraphs (A) through (C), specifically listing any medications that carried a black box warning, were prescribed for off-label use, were psychotropic, or carried warnings that included suicidal ideation.” [Emphasis added]

The bill clearly covers all psychiatric drugs.

On March 2, 2016, Congressman Jolly issued a press release which contained the following:

“‘It is critical that we understand whether there is any impact of certain psychiatric drugs prescribed for issues like P.T.S.D., depression or traumatic brain injuries, on the decision of a veteran to take their own life,’ Jolly said. ‘With veterans dying by suicide at a heartbreaking rate, we need to take a hard look at all possible factors in order to help prevent these tragedies.’

Specifically, the Veteran Suicide Prevention Act would require the VA to record the total number of veterans who have died by suicide during the past five years, compile a comprehensive list of the medications prescribed to and found in the systems of such veterans at the time of their deaths, and report which Veterans Health Administration facilities have disproportionately high rates of psychiatric drug prescription and suicide among veterans treated at those facilities.  The VA would then be required to submit to Congress a publicly available report on the results of their review, along with their plan of action for improving the safety and well-being of veterans.”

The wording of the House Bill is essentially similar to that of the Senate Bill.


Psychiatric drugs are poisons.  They poison the brains and other organs of those who take them.  In some cases, the adverse effects are slow, often taking years, or even decades, to become obvious.  But in certain cases, the poisoning is rapid and catastrophic.  The facts of this matter have been systematically suppressed by psychiatry, and by their pharmaceutical allies, for decades.

This great lie, this monumental hoax, is the soft underbelly of psychiatry.  And it is on this great lie that their self-serving drug-pushing empire will ultimately crumble.  The bills introduced by Sen. McCain and Rep. Jolly have the potential to begin this process.

I think we can be reasonably certain that at this time, psychiatry and pharma are leaving no stone unturned in their efforts to kill these companion bills.  Skids are being greased with ill-gotten largesse; favors are being called in; lawmakers in vulnerable seats are being canvassed by pharma’s check-writers; and so on.  Every effort that money can buy is being used to kill or gut these bills.

So please, if you live in the US, write to your legislators (Senate and House), and ask them to support these bills:

Senate:             S 3410             Veteran Overmedication Prevention Act

House:             HR 4640         Veteran Suicide Prevention Act

Also, please consider writing to Senator McCain and Congressman Jolly, thanking them for this initiative and outlining its importance.

Antidepressant Drugs and Suicide Rates

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Isacsson Table 1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

But the plot thickens even further:

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

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

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

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

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


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

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

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

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.”

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.

Another Survivor’s Tale

My Story
This post was submitted by a reader.

I tried to commit suicide for the first time when I was 15. I spent my 16th birthday locked up in Dammasch State Mental Hospital, I freaked out when I was told I was going to have to stay so my clothes were ripped off me, by male aids and I was thrown naked in a real padded room… hint they are NOT padded. The light was on all the time and nothing was provided for cover to keep warm. I remember seeing men looking at me and I remember pictures being taken thru the peek hole window. I was in that room, with meals shoved thru a slit in the door for 3 days. The toilet was a hole in the floor and no, there wasn’t any toilet paper. . While at the “hospital”, I remember being put in a strait jacket and tied into a chair and my “meds” forced down my throat. When I realized I could vomit them back up I was sedated and given drugs via an IV. I woke up to being raped. I made friends with one gal, she was 14. She had ( I know know as ) anorexia. I watched her try and try and try to eat. She died. Another person I made friends with hung himself and died. The psy dr said I was on the schedule for shock treatments since I refused to co-operate with the rules and the staff. That scared the shit outta me. I started doing all the things I was supposed to do and 3 months later I was released.. cured. Nothing was different for me, except I learned how to manipulate people to get what I wanted. I HATED that feeling so I never took “advantage” of that “skill”.. Remember I had just turned 16.

In my early 20’s I tried to commit suicide again and committed to another hosp in Vancouver WA with a DX of Manic Depression. I was on a cocktail of lithium, stelazine, tofranil chloral hydrate and a few others I can’t remember the names of .. for more than 7 years I saw a psychiatrist until my divorce and my insurance ran out. Dumped to fare the best I could into the mental health system for the poor I quit all my drugs cold turkey.
It was while under the Dr’s care I read a book he recommended called Self-Talk. I believed I was sick with metal illness(es?) until I read that book. For the first time I heard no one can make me feel anyway at all unless I choose to let them. That my responses to life were totally under my control and direction ALL of them. I was 32.  I’ve attempted suicide or came very very close to it 6 times in my life. Finally I asked myself, self, I’m smart enough to have gotten the job done so whats REALLY going on? I figured out WHY I kept diving into the back hole. I really do walk a different, road now thanks to getting the message my subconscious kept sending me. Thats been my experience with the Mental Health system. I am continually agast and appalled at the amount of drugs being forced onto people, particularly children, We adults have been fed a line of BS for so long about depression that it’s destroying us as a nation and no one can see it.

A  Reader

Antidepressants and Suicide

There was an interesting article, Antidepressant regulations tightened following suicide, in the Copenhagen Post on January 7.  Thanks to Mad in America for the link. It is reported that Danilo Terrida, aged 20, committed suicide in 2011

“…eleven days after he was prescribed antidepressants following an eight-minute-long conversation with a doctor.” 

The doctor has been deemed responsible for the suicide by the National Agency for Patients’ Rights and Complaints.  According to its website:

“The National Agency for Patients’ Rights and Complaints functions as a single point of access for patients who wish to complain about the professional treatment in the Danish health service.”

As a result of this case, Sundhedsstyrelsen, the Danish Health and Medicines Authority, has issued a directive requiring a more thorough assessment before these drugs can be prescribed to people aged 18 to 24.

Here are some quotes from the article:

“The case has sparked a debate about the dangers of psychiatric drugs, and in Politiken newspaper today Peter Gøtzsche, medical researcher and leader of the Nordic Cochrane Center at Copenhagen’s Rigshospitalet, wrote that antidepressants have caused healthy people to commit suicide.”

“He [Gøtzsche] added that psychiatric medication often does more harm than good and that patients would often be better off without medication.”

“‘Doctors cannot cope with the paradox that drugs that can be useful for short-term treatment can be highly dangerous when used for years and even create the illnesses that they were supposed to prevent, or even bring on an even worse illness,’ Gøtzsche wrote.”

So, we have one more piece of confirmation of something that’s been known for years.  Antidepressants increase the risk of suicide for some individuals, especially in the period immediately following initiation.  For decades, the pharmaceutical companies and the psychiatrists spun this embarrassing fact as evidence that the drugs were working.  The story went like this:  when people are deeply depressed, they lack the energy or motivation to even take their own lives.  But as the antidepressant “kicks in,” the person begins to feel more motivation, though still considerably depressed.  So he kills himself.

And psychiatry actually embraced and promulgated that nonsense.  Today it is clear that the drugs, especially the serotonin boosters, actually generate suicidal thoughts and intentions in some individuals, especially young people.

Requiring a more thorough assessment, as the Danes plan to do, seems a fairly minimal precaution, but it’s better than the 8-minute conversation that Danilo Terrida got.  The ongoing problem, however, is that there is, as far as I know, no way to identify those people who pose particular risk in this regard, other than intensive individualized monitoring for all people who are prescribed these products.  It seems unlikely that screening of that magnitude will become general practice, given the frequency with which antidepressants are being prescribed.  So instead of an 8-minute interview, there’ll be a 30-minute interview, but the results may not be much different.

In addition, this whole issue needs to be publicized more in order to ensure that clients are making informed choices.

Sandy Hook Massacre: The Unanswered Question

On December 27, 2013, Connecticut State Police issued a 7,000-page, heavily redacted, report on the massacre that occurred at Sandy Hook Elementary School just over a year earlier (December 14, 2012).  For the record, I have not read the 7,000-page report, but I have read the Wikipedia article Sandy Hook Elementary School shooting, last updated January 4, 2013, and several media reports on the matter, including reports from the New York Times, the Hartford Courant, and the Washington Post.

Obviously there is an enormous volume of material in the official reports and in the various media reports and comments.  But there is still one major unanswered question.  Was Adam Lanza under the influence of a psychopharmaceutical product(s) at the time of the shooting or in the period immediately prior to the shooting?  There is a report in the record that he took Celexa (citalopram) for a short while in 2006, but no reports of psychiatric treatment since that time.  But there are some reasons for doubt.


On August 22, 2013, Connecticut Assistant Attorney General, Patrick B. Kwanashie, during a freedom of information hearing on this matter, stated that releasing this information could “… cause a lot of people to stop taking their medications.”  He made his statement in response to AbleChild’s request for Adam Lanza’s medical records, especially with regards to any psychiatric drugs that he might have taken.  The hearing was videotaped.  Here is an excerpt, transcribed verbatim, from Mr. Kwanashie’s response.  The excerpt begins at about 1 hour 4 minutes into the tape.

“Therefore it is simply not sure that if you don’t fall into one of those categories, what you have to advance reasons that you actually do have a real interest in the [unclear] 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 uh outcome of the use of antidepressants, or thee thee thee 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 information, of that information.  You can’t generalize just from one case.  Even if you can conclusively establish that Adam Lanza, his his uh his murderous actions, were caused by antidepressants, you can’t logically from that conclude that um um in others would uh, would uh commit the same actions as a result of taking antidepressants.  Um, um, 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, um it is harmful, because you can cause a lot of people um to stop taking their medications, stop cooperating with their treating physicians, um um just because of the heinousness of uh what Adam Lanza did.  As thee, as thee thee material, the FDA material that they submitted show, it would take a lot of studies uh over a long period of time and among, and within various demographic groups to even begin to uh establish causal links between antidepressants and uh uh aggressive actions or suicidal behavior.  And thee thee informed uh uh, the informed opinion has not quite reached that the point to to say definitively that there’s a causal link between uh between uh the use of antidepressants and uh and uh violent behavior.  Having correlations, there are correlations, but to say there are correlations doesn’t necessarily mean there is, the relationship is causal.  And uh uh this is an issue the FDA is still grappling with, and so far it’s been willing to do is is ask the drug makers to put warnings on their on their products and to advise physicians, treating physicians, to follow monitor their uh their  uh patients closely uh uh at the uh the beginning of uh uh the taking of antidepressants.  Um so it’s a complex issue, um and to pretend that you can just based on this one case make uh recommendations as to how people should uh uh how we 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 the source of mischief.”

The hesitancies make the material a little difficult to read, but I think the message is clear:  AbleChild should be denied access to the documents in question because they are likely to draw and publicize unwarranted assumptions from these documents, and this might induce large numbers of people to stop taking the drugs in question.

Mr. Kwanashie’s statement is extraordinary for three reasons:

1.  The issue on the table was whether or not AbleChild had a “legitimate interest” (as defined by the statute and regulations) in the material.  This was essentially a legal/technical matter, and the complainant’s attorney Jonathan Emord had outlined various legal reasons in support of their right to the information.

What appeared to be expected from the Assistant Attorney General, who represented the State of Connecticut, was a rebuttal also based on legal issues and technicalities.  Instead, he launched gratuitously into these controversial waters, and provided, in my view, a glimpse of what seems to be going on behind the scenes.

It is of note that when he had finished these remarks, the hearing chairperson drew him back to the legal issues and asked him some clarificatory questions on those matters.

2.  Mr. Kwanashie has unquestionably conveyed the impression that there is some information that is being suppressed, and that it is being suppressed for the reasons that he outlined; i.e. so that people would not stop taking their pills.

3.  Mr. Kwanashie was not speaking as a private individual, but rather as the representative of the State of Connecticut.  He had almost certainly been authorized by his superiors to make the statement in question, and presumably the statement reflects the state’s stance on this issue generally, i.e. not just in the Adam Lanza case.

It’s possible, of course, that Mr. Kwanashie was confused or inadequately prepared for the hearing.  But that seems unlikely.  He is 59 years old, has been licensed to practice law in Connecticut since 1988, and draws a salary of $142,000.  Denying a freedom of information request is not a trivial matter, and the notion that he would go to such a hearing unprepared is hard to credit.  This is especially the case in that the Lanza shooting is probably the highest profile case that the State of Connecticut has encountered in decades.

So what we have is a credible indication that Adam Lanza was taking psychoactive “medication” around the time of the murders.  But the State of Connecticut will not release this information because such a release might induce large numbers of people to stop taking antidepressants.


A December 13, 2013, article called Newtown One Year Later, The Missing Link on the AbleChild site contained a link to a video.  The video is of a town hall meeting that Minnesota Congresswoman Betty McCollum held with some of her constituents in Oakdale, Minnesota eleven months earlier, on January 26, 2013.  At about 39 minutes and 30 seconds into the video, a member of the audience made the following comments:

“…I agree with Congresswoman McCollum that we need to have a dialogue with what’s going on with these gun issues.  I’m, we’re blindly running into gun control and a violation of the second amendment – but we’re not even sure if we have a  gun control problem.  I’ve been reading things where a lot of these kids – the Sandy Hook kid and the kid up in Red Lake Minnesota and Aurora – they’re all on Prozac and Ritalin and is this a psychopharmaceutical issue that’s causing these kids to do. – I mean – I think we need to have a,  I think we need to bring not only with both sides of the aisle but both sides of the issue together and examine exactly what’s going on here.  Is this a gun problem or is it a – you know – it could be anything.  But I think before we jump into legislating one portion of this we need to examine the entire issue and find out what’s going on.  Thank you very much.”

Here’s Congresswoman McCollum’s verbatim response:

“To that, let me tell you something: that, to quote my grandmother (so I use nice words here), frosted my cookies.  We can’t study, federally – we’re prohibited from studying the effects of some of the drugs that you were just talking about as it relates to people who go out and commit violent acts with guns.  We’re prohibited from studying that.  It’s an NRA square bolt.  That’s why I’d never be at 100%.  I think we have an obligation to study those kinds of issues.  So that’s why we need a dialogue.  It is prohibited from the CDC – the Centers of Disease Control – to study this.  It’s wrong!  And that’s why we need to get the lobbying efforts out of the discussion, just saying here’s your scorecard and they only highlight certain issues.  And they don’t give you everything else that they’re involved in. And that’s why I’m here and that’s why I’m glad you’re here.  So that we can talk and listen to one another.  And so I really am feeling very good that you’re here today.”

In the December 13 article, AbleChild describe their unsuccessful attempts to obtain additional information from Congresswoman McCollum concerning the CDC “rule.”

My interpretation of the Congresswoman’s words in the town hall meeting is that there is some kind of prohibition within the government on researching this topic, and that this prohibition is connected to lobbying – presumably by the pharmaceutical industry.

According to Wikipedia, Congresswoman Betty Louise McCollum is 59 years old, and is the U.S. Representative for Minnesota’s 4th congressional district, serving since 2001. She is a member of the Democratic-Farmer-Labor Party (DFL).  She currently serves on the United States House Appropriations Committee and the following subcommittees:  Subcommittee on Interior, Environment and Related Agencies, United States House Appropriations Subcommittee on Defense.   She also previously served on the House Committee Education and the Workforce; House Committee on Government Reform; House Committee on Resources; and House Committee on the Budget.  So she is mature and not, I imagine, given to flights of fancy.  She appears credible; she seems to have some personal knowledge of the “rule”; and there is nothing to suggest that she is making this stuff up.

Why is the media not all over this?  The town hall meeting was held almost a year ago.  To date the video has had only 307 hits.


And let’s not forget that a petition to formally investigate the link between psychopharmaceutical products and violence was removed from the White House petition website in December of 2012 without explanation, even though it was well on the way to obtaining the requisite number of signatures.

Is the US government, or any branch, or agency, of the US government deliberately suppressing research into the widely-suspected link between psychopharmaceutical products and mass shootings?  And if so, is this suppression the result of pharmaceutical lobbying?

If in fact, as many of us suspect, there is a causal link between the mass shootings and psychopharma products, shouldn’t this be a matter of urgent national importance?  Whose interests would be served by the suppression of this information?  Has the constitutional supremacy of We The People been usurped by They The Drug Companies?  By what distorted “logic” can a government collude with the notion of keeping people in the dark concerning a devastating drug effect in order to ensure that individuals keep taking these drugs?  I encourage my readers to check out both videos, and perhaps recommend that your friends and contacts do the same.  Perhaps there’s an innocent interpretation to all this.  If so, I’d be very grateful if someone could explain it to me.


In 2000, Joseph Glenmullen, MD, a psychiatrist, published Prozac Backlash – a critical look at the adverse effects of Prozac and other serotonin boosters.  Here’s a quote from the final chapter:

“We do know, from documented clinical experience and research, that these drugs have led to suicidal and violent urges in some patients.  We desperately need warnings for patients and doctors, together with information on prevention and coping with suicidal and violent impulses when they occur.  Additional research to help us understand the phenomenon is desirable but should not be merely a ploy to delay such warnings and preventive steps.” (p 336)

And that was more than 13 years ago!

CAFÉ Study: Real Science or Marketing Exercise?


On December 8,  I received the following question from a reader:  (The subject matter is the controversial CAFÉ – Comparisons of Atypicals in First Episode of Psychosis – study.  This was the study in which Dan Markingson committed suicide.)

“It appears that there was no head-to-head with a control group taking a placebo pill. Nor was there a control group featuring ‘old’ types of ‘antipsychotic’. If that was the case then it is very poor study. If you are just looking at 3 ‘new’ subtypes of a ‘new’ class – then what on earth can you hope to show from the data.”

I started to write a response, but the subject is complex, and my response became the following article.


Any discussion of CAFÉ must begin with a review of CATIE (Clinical Antipsychotic Trials of Intervention Effectiveness).

CATIE was a randomized trial funded by the US government (NIMH).  It was written up in three phases:  Phase 1 (Lieberman J et al, 2005); Phase 2 Part a (McEvoy JP et al, 2006) and Phase 2 Part b (Stroup TS et al, 2006);  and CATIE Phase 3 (Stroup TS et al, 2009).  CATIE’s purpose was to compare old neuroleptics with new neuroleptics.  There was no placebo.  This reflected the belief/assumption that the efficacy of neuroleptics generally had already been established.  The researchers compared the old drug perphenazine with the second generation neuroleptics olanzapine, quetiapine, risperidone, and ziprasidone.  The conclusion:

“Olanzapine was the most effective in terms of the rates of discontinuation, and the efficacy of the conventional antipsychotic agent perphenazine appeared similar to that of quetiapine, risperidone, and ziprasidone.  Olanzapine was associated with greater weight gain and increases in measurers of glucose and lipid metabolism.” (Phase 1, p 1209)

So, a kind of mixed result; but notice that quetiapine was shown to be no better than the old drug.

In CATIE phase 2, clozapine was introduced.  One of the findings was:

“At 3-month assessments, Positive and Negative Syndrome Scale total scores had decreased more in patients treated with clozapine than in patients treated with quetiapine or risperidone but not olanzapine.” ( Part a, p 600)


“…risperidone and olanzapine were more effective than quetiapine and ziprasidone as reflected by longer time until discontinuation for any reason.” (Part b, p 611)

Again, a mixed result.  Clozapine is most effective but known to have even more serious adverse effects than other neuroleptics.  But notice again that quetiapine isn’t looking too good.

CATIE also had a placebo-controlled arm that addressed the use of neuroleptics in “treating” aggression and agitation in patients with Alzheimer’s Disease (CATIE-AD, Schenider et al 2006).  Even here, quetiapine didn’t do so well.  It had the lowest “improvement” rate, though the differences were not statistically significant.  The researchers also noted that:

“Adverse effects offset advantages in the efficacy of atypical antipsychotic drugs for the treatment of psychosis, aggression, or agitation in patients with Alzheimer’s disease.” (p 1525)

It was also found in CATIE Phase 1 that the individuals who had received quetiapine had the highest rate of hospitalization during the study.  The comparative figures were:

Olanzapine –    11%
Quetiapine –    20%
Risperidone –   15%
Perphenazine – 16%
Ziprasidone –   18%
(Table 3, p 1220)

These differences were statistically significant at the 0.001 level (i.e. there’s less than one chance in a thousand that the differences could have occurred by chance).


Which brings us to CAFÉ, a multi-site study of neuroleptic treatment of first episode psychosis, funded by AstraZeneca, manufacturer of quetiapine (Seroquel).  CAFÉ was written up in two parts in the American Journal of Psychiatry.  CAFÉ has been criticized as little more than a marketing ploy by AstraZeneca to rescue their baby from the CATIE fall-out.

There were two main hypotheses:

“…that quetiapine was not inferior to olanzapine or risperidone in the rate of all cause treatment discontinuation in early psychosis patients.” (p 1050)


“…that the three agents would be equivalent in their effects on various neurocognitive measures.” (p 1061)

The researchers concluded:

“Olanzapine, quetiapine, and risperidone demonstrated comparable effectiveness in early-psychosis patients, as indicated by similar rates of all-cause treatment discontinuation.” (p 1050)


“Olanzapine, quetiapine, and risperidone all produced significant improvement in neurocognition in early-psychosis patients.  Although cognitive improvements were modest, their clinical importance was suggested by relationships with improvements in functional outcome.” (p 1061)

So, quetiapine is just as good, as measured by rates of treatment discontinuation, in early stage psychosis as the other second-generation neuroleptics.  The rate of treatment discontinuation, however, is a fairly minimal outcome criterion.  The usual rationale for using it in these kinds of studies is the assumption that it is inevitably associated with poor outcome generally.  This assumption has been critiqued widely in recent years, but is still generally accepted by psychiatrists.

But the most serious critique launched against CAFÉ is that the researchers administered the rival drugs at reduced dosages.  Olanzapine and risperidone were administered at about 60% of the CATIE dose, while quetiapine was administered at about 90% of the CATIE dose.  Here’s what the researchers wrote:

“Previous studies suggesting that first-episode patients receive therapeutic benefit from antipsychotic doses lower than those required for chronic patients and that first-episode patients develop unnecessary extrapyramidal side effects at higher doses led us to use lower dose ranges of olanzapine and risperidone in this study than those used in the Clinical Antipsychotic Trials of Intervention effectiveness (CATIE). However, given quetiapine’s low extrapyramidal side effects liability, we expected that the quetiapine doses used in CATIE would be tolerable in our study population.” (p 1058)

This seems questionable.  Neuroleptics, at least initially, reduce agitated thoughts and behavior.  And the higher the dose, the greater the “improvement.”  The authors themselves acknowledged this interpretation:

“This may have been a factor in the comparable effectiveness demonstrated by quetiapine.  In the CATIE phase 1 and phase 2 schizophrenia trials…higher mean modal doses of olanzapine and risperidone but similar mean modal doses of quetiapine were used; in these trials, olanzapine and less consistently risperidone proved to be more effective than quetiapine.  It remains an empirical question whether higher doses will improve the relative effectiveness of quetiapine in chronic patients.” (p 1058)

But this is buried in the text of a 20-page article.  As mentioned earlier, the article is written up in two parts in the American Journal of Psychiatry, 2007 (p 1050-1060 and p 1060-1071).  The above quotes appear on page 1058, but are not reflected in the conclusions.

The authors’ assertion of “low extrapyramidal side effect liability” for quetiapine is also of interest.  Firstly, they cite no reference in support of this assertion.  Secondly, CATIE had reported the following percentages for extrapyramidal effects: olanzapine 2%; quetiapine 3%; risperidone 3%; ziprasidone 4%.  The actual numbers are too small to draw firm conclusions, but there is nothing to suggest that quetiapine has a particularly low liability.

Another item of interest that was buried in the text, but did not appear in the conclusions, was:

“A total of 18 serious adverse events occurred, four in the olanzapine group and seven each in the quetiapine and risperidone groups.  These events included two suicide attempts and one alleged homicide in the olanzapine group, two completed suicides and one case of suicidal ideation in the quetiapine group, and one suicide attempt in the risperidone group.” (p 1057)

Further indications of the researchers’ agenda are suggested by the following quote:

“Our findings in this study suggest that the effect of quetiapine on cognition may be as beneficial as that of olanzapine or risperidone, and thus this agent may be another evidenced-based alternative for clinicians who focus on cognitive outcomes. (p 1069)

Even one of the primary conclusions was tenuous.  In the second part of the write-up, as mentioned earlier, the authors had concluded:

“Olanzapine, quetiapine and risperidone all produced significant improvements in neurocognition in early-psychosis patients.” (p 1061)

Buried in the text, however, on page 1069-1070, they wrote:

“In this study, patients with early psychosis who demonstrated cognitive improvement at 52 weeks also demonstrated functional benefit in social and occupational domains, which suggests a functional relevance for cognitive improvement.  One caveat to this promising conclusion is that given the high dropout rate in this study, these data apply only to the patients who were able to stay in treatment and complete comprehensive assessments for 52 weeks, a group that comprised only 20% of the original sample.” [emphasis added]


As mentioned earlier, the outcome criteria that were highlighted in the conclusions sections of the two papers were:  rate of treatment discontinuation and improvements in neurocognition.

However, various other items were assessed during CAFÉ that might usefully have been included in the papers’ conclusions.  In fact, the authors stated:

“Efficacy was measured in two domains:  1) psychopathology and 2) social and occupational functioning.  Psychopathology was assessed by the PANSS, the CGI, and the Calgary Depression Scale for Schizophrenia….  Social and occupational functioning was assessed with the Heinrichs-Carpenter Quality of Life Scale….” (p 1053)

Measurements on these scales were taken before the study began, and at 12 and 52 weeks.  The results are presented in Table 2 (p 1052).    (Click on the image below to see the full-size table.)  This is a rather complex table, and comparisons across the three drugs are not easy.  For this reason, I restructured and graphed the data below.

Table 2 from CAFE Study





In Table 2, an improvement in some of the scales is indicated by a negative number, in other scales by a positive number.  For ease of comparison, I eliminated the signs and focused only on the magnitude of change from the baseline value.  In each graph the direction upwards on the page indicates more improvement from baseline.  As can be readily seen, the level of improvement with quetiapine is lower (at both 12 and 52 weeks) than with olanzapine or risperidone in 6 of the 7 scales.  This difference is marginal in the CGI Severity Scale, and only reached statistical significance with the PANSS positive symptoms scores (and this was mentioned in the abstract), but the fact that quetiapine fared worse on 6 of the 7 variables seems noteworthy.

This is especially true in that the six scales addressed here are precisely the measures that would be of particular interest in the assessment of treatment effectiveness for psychotic thoughts/behaviors.  In fact, CATIE used the PANSS positive and negative scales to assess effectiveness.  Since the entire purpose of the study was to compare the relative effectiveness  of these drugs, it’s difficult to find a valid reason for not presenting the relative effectiveness data more clearly

[visualizer id=”3797″]

[visualizer id=”3792″]

[visualizer id=”3800″]

[visualizer id=”3801″]

[visualizer id=”3802″]

[visualizer id=”3803″]

[visualizer id=”3804″]


The big question is:  was CAFÉ a piece of genuine scientific research; or was it a marketing exercise bought and paid for by AstraZeneca in an attempt to rehabilitate their drug quetiapine (Seroquel)?  Obviously arguments can be made on both sides, but here are two factors that may have some bearing.

1.  AstraZeneca funded the study.

2.  There were a total of twelve authors listed on the two write-ups.  All but three declared a history of financial ties to AstraZeneca.  Of these three, Dr. Lieberman acknowledged that he had worked for AstraZeneca as an unremunerated consultant.  Dr. Sweeney declared only the funding for the present study (he was lead investigator), and Dr. Gu declared no ties.  Two of the authors, Dr. Lazarus and Dr. Sweitzer were employees of AstraZeneca, and both held stock options. (p 1059 and 1070)

The importance of these kinds of funding issues was highlighted in a study of head-to-head comparisons of second generation neuroleptics by Heres et al (Amer Jour Psych 2006).  These researchers found:

“In 90.0% of the studies, the reported overall outcome was in favor of the sponsor’s drug….Potential sources of bias occurred in the areas of doses and dose escalation, study entry criteria and study populations, statistics and methods, and reporting of results and wording of findings.”


There were two completed suicides in the study, both in the quetiapine group.  One of these was Dan Markingson.  Dan’s inclusion in the study has been the subject of considerable controversy.  His mother, Mary Weiss, stated that she saw his condition deteriorate markedly during the period in question, and that she made repeated attempts to have him removed from the study and taken off the drug.  It is also reported that she alerted the study coordinator to the danger of homicide or suicide.  Her protests were not heeded.  Recently, thanks largely to the persistent efforts of Carl Elliott, the Faculty Senate of the University of Minnesota has voted to commission an independent inquiry into the circumstances of Dan’s death.  However, on December 11, Eric Kaler, President of the university stated in a press interview that the inquiry will only be looking into the university’s review procedures and that it will not be a review of Dan Markingson’s death.  This announcement, predictably, has re-opened the controversy (subsequent letter from University of Toronto).


Why did the research team at the University of Minnesota’s Department of Psychiatry not take protective action in response to Mary Weiss’s warnings concerning her son Dan?

Did they discuss these concerns, and, if so, is there a record of these discussions?

Was an assessment made of Dan’s suicide potential in response to Mary’s expressions of concern?  If so, what was the result of that assessment?

On which site(s) did the other suicide and the three suicide attempts occur?

Was the decision-making concerning Dan influenced by the desire to portray quetiapine in as favorable a light as possible?  In particular, was the decision not to hospitalize Dan influenced by the fact that quetiapine had fared so poorly in CATIE on the hospitalization measure?

With regards to this last point, there is, I suggest, a pressing need to separate and publish CAFÉ’s relative hospitalization rates for the three drugs.  This information was not published in the study write-up, but presumably would still be available in the research files.

It is also important to investigate the question of informed consent.  In the study write-up, the authors state that:

“…written informed consent was obtained from the patients or their legally authorized representatives.” (p 1051)

It has been suggested that Dan Markingson was incapable of providing informed consent at the time of his enrollment.  Carl Elliott has written:

“When Mary found out that Dan had been recruited into the CAFE study, she was stunned. “I do not want him in a clinical study,” she told Olson [Stephen C. Olson, MD, one of the researchers]. Just a few days earlier, Olson indicated in a petition to the court that Dan was both dangerous and mentally incapable of consenting to antipsychotic medication. How could he now be capable of consenting to a research study with the very same antipsychotics—especially when the alternative was commitment to a state mental institution?”

A complicating factor here is that AstraZeneca paid the University of Minnesota $15,648 for each person they enrolled in CAFÉ, and it has been suggested that this financial incentive might have clouded the researchers’ judgment with regards to the ability to provide informed consent.

At the very least there are unanswered questions.  Was Dan capable of giving informed consent?  Was his “consent” coerced in any way?

It is now over nine years since Dan’s death.  It is high time that these questions were addressed in a serious and impartial manner.


Psychiatry and Suicide Prevention: A 30-year Failed Experiment

There’s an interesting article on Mad in America dated September 17, 2013.  It’s titled Psychiatry & Suicide Prevention: A 30-year Failed Experiment, and was written by Maria Bradshaw.

Maria Bradshaw is the founder of CASPER, an organization that rejects the medical model of suicide prevention in favor of a sociological model.  Ms. Bradshaw founded CASPER after her son’s antidepressant-induced suicide.

Here’s the gist of Ms. Bradshaw article:

Roger Mulder, MD, is head of psychiatry at Otago University in New Zealand.  For at least the last 15 years, he has supported the notion of psychiatric intervention as a suicide-prevention measure.  For instance, here’s something he wrote in 2008 in an article published in Acta Psychiatrica Scandinavica:

“Suicide behaviours are common in depressed out-patients.  Antidepressant treatment is associated with a rapid and significant reduction in suicidal behaviours. The rate of emergent suicidal behaviour was low and the risk benefit ratio for antidepressants appears to favour their use.”

However, at a conference in Auckland, New Zealand, two weeks ago, he stated that the psychiatric model of screening people for suicide risk was not effective.  The conference was covered by Simon Collins of the New Zealand Herald.  Here’s a quote from Dr. Mulder:

“‘We’ve had a 20- or 30-year experiment which hasn’t worked.'”

In her article, Ms. Bradshaw compliments Dr. Mulder on having the integrity to alter his stance in the light of the evidence.  In his conference presentation, Dr. Mulder had pointed out that targeting groups deemed to be at high risk with psychological/pharmacological interventions has failed to impact actual suicide rates.

Ms. Bradshaw herself argues that not only has the psychiatric paradigm failed to lower suicide rates, it has actually caused them to increase.

In support of this position, she points out that the suicide rate for people who have used mental health services in the past year is 137.6 per 100,000, but only 7.6 per 100,000 for those who have not had a mental health contact.  Ms. Bradshaw doesn’t cite a source for these figures, but the study is almost certainly not a randomized controlled trial.  So to some extent, we may be comparing apples to oranges.  But the numbers are sobering nonetheless, especially since the “life-saving” aspect of antidepressants is frequently touted by psychiatrists in response to various criticisms.

Another interesting statistic that Dr. Mulder reportedly mentioned at the conference is that “only 3 percent of those labeled as ‘high risk’ actually killed themselves, while 60 per cent of actual suicides had been categorized as ‘low risk.'”  [Quoted from the Simon Collins article in the New Zealand Herald.]


It has long been recognized that a person’s risk for suicide increases in the first few weeks (months?) of taking an antidepressant.  The psychiatric explanation of this was that the putative therapeutic action of the drug gave the individual sufficient motivation to do what he had been wanting to do previously – namely to take his own life.

I’ve never been impressed with this argument, and in my view, it’s becoming increasingly clear that the so-called antidepressants do in fact induce or strengthen suicidal urges in some people.

Maria Bradshaw’s article is well worth reading.  CASPER, the organization she founded after her son’s suicide, is also worth watching.  One of the ideas they are developing is the training of potential natural helpers in how to respond to people who mention suicide.  The New Zealand Herald article describes how Ms. Bradshaw provided training in these matters to a group of hairdressers.

It’s too early to say how successful these kinds of endeavors will be, but the idea of natural helpers has, in my view, enormous potential, not only with regards to suicide prevention, but also in helping people cope with problems generally, and develop new skills.