Tag Archives: neuroleptics

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.

“DANGERS OF FLUPHENAZINE

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.”

and

“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.

OTHER SIMILAR REPORTS

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.”

CASE  NO. 1

“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:

CASE NO. 2

“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]

CASE NO. 3

“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.

AKATHISIA AND ANTIDEPRESSANTS

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.”

and

“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.”

and

“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”

and

“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.”

and

“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?

DSM AND AKATHISIA

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]

and

“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.

FINALLY

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?

INCIDENTALLY

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).

Allen Frances on the Benefits of “Antipsychotics”

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Back to the Treatment Guidelines document:

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

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

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

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

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

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

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

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

Psychosocial intervention

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

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

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

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

Back to Dr. Frances’s current article:

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

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

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

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

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

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

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

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

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

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

Allen Frances ‘Replies’

BACKGROUND

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

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

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

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

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

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

. . . . . . . . . . . . . . . . 

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

So, to set the record straight:

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

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

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

This challenge still stands.

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

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

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

Allen Frances’ Ties to Johnson & Johnson

INTRODUCTION

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

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

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

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

PSYCHIATRISTS FOR HIRE

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

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

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

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

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

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

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

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

Here are some quotes from David Rothman’s report:

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

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

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

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

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

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

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

Back to Paula Caplan’s article:

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

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

And another quote from David Rothman:

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

. . . . . . . . . . . . . . . . 

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

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

ALLEN FRANCES REPLIES

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Ah!  That explains everything.

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

But then, Dr. Frances acknowledges some retrospective misgivings:

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

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

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

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

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

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

PUBLICATION OF THE GUIDLELINES

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

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

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

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

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

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

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

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

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

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

A CHALLENGE TO DR. FRANCES

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

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

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

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

AND INCIDENTALLY

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

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

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

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

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

Such a sense of civic responsibility!

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

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

FINALLY

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

AHRQ fig 1 on antipsychotics

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

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

Neuroleptic Drugs And Mortality

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

The authors offer the following background for the study:

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

and the following conclusions:

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

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

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

Torniainen fig 1 upper half

 

 

 

 

 

 

 

 

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

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

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

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

The actual numbers are:

Tornianen hazard ratio chart

 

 

 

 

 

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

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

The numbers of people who died in each group were:

Tornianen study Death rates

 

 

 

 

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

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

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

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

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

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

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

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

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

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

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

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

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

The results for the first comparison were:

Tornianen first comparison.

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

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

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

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

MORTALITY RATES AND NEUROLEPTIC USE

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

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

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

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

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

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

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

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

Torniainen Table 3

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

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

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

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

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

Tornianen causes of death charge

 

 

 

 

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

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

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

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

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

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

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

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

PRESENTATION OF DATA

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

Torniainen Fig 2

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

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

Tornianen Mortality composite change data

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

AUTHORS’ CONCLUSIONS

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

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

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

AND INCIDENTALLY

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

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

In the present paper it is acknowledged:

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

CITATIONS

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

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

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

And schizophrenia.com:

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

And Joanna Lyford writing on Medwire News:

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

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

The Drugging of Children in Foster Care

It’s no secret that here in America, foster children are being prescribed psychiatric drugs, especially neuroleptics, as a means of controlling their behavior.  A great deal has been said and written on the matter.  Politicians have declared the practice deplorable.  Children’s advocacy groups have expressed concern, and, of course, those of us in the antipsychiatry movement have screamed till we’re hoarse.  But the problem persists. 

For the past six months or so, the San Jose Mercury News, a California newspaper, has been running frequent articles on this topic, calling for oversight and corrective action.

On February 24, 2015, Karen de Sá, a reporter with that newspaper, published an article titled Senate panel examines why California foster care system ‘addicted’ to psychiatric drugs.  It’s an excellent article, which highlights various aspects of the problem, and provides updated information on this matter.

Here are some quotes:

“California’s foster care system ‘has grown more addicted to mind-altering medication,’ the chair of a powerful Senate committee told a packed public hearing in the state Capitol on Tuesday, adding that ‘here in California, we’ve done little to act on this alarming issue.'”

“Lightbourne said two state-sponsored panels have spent years working to develop guidelines that would protect foster children from the excessive use of psych medications and to house fewer kids at residential group homes, where drugs are most frequently prescribed. Foster children deserve ‘nonmedical treatments whenever possible,’ Lightbourne said.”

“‘We need to shift our thinking away from the primacy of psychiatric medications toward relationships,’ testified George Stewart, a Berkeley child psychiatrist who has spent much of his career tapering severely traumatized children safely off high-risk drug cocktails. ‘We are going to look back on this era of great enthusiasm for psychiatric medications and either scratch our heads or beat our heads. We will look back in 20 years and say, ‘What were we doing?'”

“Senators also said they were alarmed by the newspaper’s analysis that showed how pharmaceutical companies lavish the state’s foster care prescribers with millions of dollars for meals, gifts, travel, speaking engagements and research grants — a practice Lightbourne called ‘deeply troubling.’ The newspaper found the doctors who prescribed the most, typically were rewarded the most.”

All of which tells a familiar story.  Pharma-psychiatry systematically targets foster children as potential customers.  They do this because the residents of foster homes, group and individual, are a “captive audience,” in the sense that the foster parent or staff member will ensure that the resident takes the pills.  In this way, non-compliance – the great drain on pharma revenue – becomes a non-issue.

Karen de Sá’s article is cogent, articulate, and powerful, and undoubtedly she and her colleagues are raising awareness on this matter.  But there was one paragraph in her article that I felt warranted some additional discussion.

“Tuesday’s four-hour hearing before the Human Services Committee highlighted a package of bills being introduced this month, following this newspaper’s investigation ‘Drugging Our Kids,’ which revealed nearly one in four foster care teens take psychiatric drugs — often to control behavior, not to treat mental illnesses. Most are prescribed antipsychotics, a powerful class of psychiatric drugs with the most harmful side effects.”

Note the phrase  “…often to control behavior, not to treat mental illnesses”.  What the author is missing here is that, within psychiatry’s spurious domain, misbehavior is a mental illness.  In fact, it is several mental illnesses.  If a child is frequently defiant, he has a mental illness called oppositional defiant disorder.  If he is given to outbursts of anger, he has a mental illness called intermittent explosive disorder.  If he is given to violating rules or infringing on the rights of others, he has a mental illness called conduct disorder.  If he is given to setting fires, he has a mental illness called pyromania.  If he is persistently angry and given to very frequent temper tantrums, he has a mental illness called disruptive mood dysregulation disorder.  And, of course, if he is disruptive and inattentive in the classroom, he has attention deficit hyperactivity disorder.  If the child’s misbehavior can’t be shoe-horned neatly into any of these categories, psychiatry has two residual categories:

  • other specified disruptive, impulse-control, and conduct disorder; and
  • unspecified disruptive impulse-control and conduct disorder.

Contrary to popular opinion, no neurological pathology is required to establish these “diagnoses.”

So, by neatly re-labeling every conceivable kind of misbehavior as a mental illness, psychiatry has established turf in this field, and has legitimized the use of drugs to “treat” this misbehavior.

This is the crux of the entire debate.  There is literally no significant problem of thinking, feeling, and/or behaving that is not listed, either directly, or by implication, in the DSM.  So, Karen de Sá is incorrect.  In the looking-glass world of psychiatry, practitioners are not prescribing major tranquilizers to control children’s behavior.  Rather, they are “treating mental illnesses”, with medications that have been proven by highly questionable pharma research to be “effective and safe”.  We have actually reached the position in our society where a physician who does not follow these practices could be held liable for failure to treat.

And this is the problem.  Every attempt to eliminate, or even reduce, this widespread and persistent practice, is doomed to failure as long as psychiatry’s spurious diagnoses are accepted as bona fide illnesses.  Because if childhood misbehavior is an illness, then psychiatrists and other physicians are not using drugs to control behavior, rather they are “treating”, compassionately and effectively, these “disabling illnesses”. 

Psychiatry, over the past five decades, has systematically and deceptively pursued a self-serving policy of medicalizing virtually every significant problem of thinking, feeling, and/or behaving.  Their pharma allies have provided the money, and psychiatry has provided the credentials, in what is arguably the most widespread and destructive swindle in human history.  And they have been enormously successful.  Their spurious notions are widely accepted today as reality.

No significant progress will be possible in these areas until the swindle is finally and utterly exposed, and sanity is restored to our conceptualizations of human activity.  Until then, despite the protests of politicians, advocates, journalists, and others, the pharma-psychiatry maw will remain wide open, and the ranks of “the mentally ill” who need “treatment” will continue to grow.

 

Thomas Insel: “Are Children Overmedicated?”

Thomas Insel, MD, is the Director of the National Institute of Mental Health.  In June of last year, he published, on the Director’s Blog, an article titled Are Children Overmedicated?  The gist of the article is that children are not being overmedicated, but rather that there is an increase in “severe psychiatric problems” in this population.

Here are some quotes, interspersed with my comments.

“The latest estimate from the National Center for Health Statistics reports that 7.5 percent of U.S. children between ages 6 and 17 were taking medication for ’emotional or behavioral difficulties’ in 2011-2012. The CDC reports a five-fold increase in the number of children under 18 on psychostimulants from 1988-1994 to 2007–2010, with the most recent rate of 4.2 percent. The same report estimates that 1.3 percent of children are on antidepressants. The rate of antipsychotic prescriptions for children has increased six-fold over this same period, according to a study of office visits within the National Ambulatory Medical Care Survey. In children under age 5, psychotropic prescription rates peaked at 1.45 percent in 2002-2005 and declined to 1.00 percent from 2006-2009.”

Dr. Insel points out that psychiatrists, parents, schools, and drug companies are often blamed for these increases. He challenges these perspectives.

“…most of the prescriptions for stimulant drugs and antidepressants are not from psychiatrists.”

This is a frequently-heard psychiatric assertion, but it is beside the point.  It is indeed the case that GP’s and various medical specialists prescribe psychiatric drugs for various problems of thinking, feeling, and/or behaving, but they can only do so because psychiatry has developed and promoted the fiction that these problems are illnesses, and the drugs are medications.  In fact, it’s even worse than that.  Psychiatry’s spurious medicalization of all human problems of thinking, feeling, and/or behaving has been so thoroughly integrated into mainstream medical care, that a physician who doesn’t prescribe psychiatric pills in certain situations could find himself legally liable for malpractice in the event of an adverse outcome.

Dr. Insel provides equally facile reasons why parents, schools, and drug companies are not to blame for the increased drugging of children. And with that whole issue out of the way, he continues:

“If psychiatrists, parents, schools, or drug companies are not the culprit, who is? The answer is potentially more complicated and more worrisome. Is it possible that the increased use of medication is not the problem but a symptom? What if more children were struggling with severe psychiatric problems and actually the problem was not over-treatment but increased need? Surely, if we discovered more children were being treated for diabetes or immune problems, we wouldn’t blame the providers or the parents. We’d be asking what drives the increase in incidence.”

Note how Dr. Insel equates psychiatric problems with real illnesses such as diabetes and immune problems.  The big difference, of course, is that real physicians don’t invent the illnesses they treat, as do psychiatrists.  Yes, more children today are “struggling with severe psychiatric problems”, but the primary reason for this is that pharma-psychiatry has been so successful in promoting the notion that virtually every problem that a child could display is an illness which needs to be “treated” with psychiatric drugs.  Former generations regarded childhood temper tantrums as a problem that needed to be addressed by parents using the normal time-honored ways.  Today these temper tantrums are a “symptom” of “disruptive mood dysregulation disorder”, a severe “psychiatric illness” warranting the attention of psychiatrists and the prescription of drugs.  There is, in fact, no difference between the temper tantrums of former years and disruptive mood dysregulation disorder of today. All that’s changed is that psychiatry has, once more, expanded its turf through the simple expedient of creating yet another “illness” by voting it into existence.  Similar observations apply to childhood inattentiveness, defiance, misconduct, boredom, etc…

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

“Skepticism regarding increased rates of emotional and behavioral difficulties as opposed to increases in other medical disorders can be attributed in part to the absence of biomarkers or laboratory tests for psychiatric diagnosis comparable to glucose tolerance tests for diabetes or anaphylactic reactions for allergies. Absent these kinds of consistent, objective measures for mental disorders, we cannot distinguish between a true increase in the number of children affected or simply changing values or trends in diagnosis. Clearly context matters. What one parent might consider hyperactivity, another parent might consider healthy exuberance.  What physicians once called attention deficit hyperactivity disorder (ADHD), often now elicits a diagnosis of childhood bipolar disorder, leading to a 40-fold increase in prevalence from 1994-1995 to 2002-2003.”

So, skepticism regarding the increased rates can be attributed partly to the absence of biomarkers.  This is true, but it is not the central issue.  The central issue is that for at least the last fifty years, organized psychiatry’s primary agenda has been the medicalization of all significant problems of thinking, feeling, and/or behaving.  They have asserted, without evidence, that these problems are illnesses and have even concocted baseless neurological pathologies as putative causes of these so-called illnesses.  By comparison, the absence of biomarkers or lab tests is a trivial issue.

And note the extraordinary dexterity with which Dr. Insel trivializes the 40-fold increase in the prevalence of “childhood bipolar disorder”.  This increase was driven largely by the efforts of Joseph Biederman, MD, and caused such a scandal that the APA created the label “disruptive mood dysregulation disorder” for the express purpose of reducing the use of the bipolar label.  This whole business was a very black chapter in a profession not noted for its moral or intellectual integrity, and resulted not only in a 40-fold increase in the “diagnosis of bipolar disorder”, but also an unprecedented increase in the prescription of neuroleptic drugs to children.  But Dr. Insel spins Dr. Biederman’s excesses as comparable to two parents holding different views as to the significance of a child’s hyperactivity.  Oh my!  What a fuss about nothing!

And incidentally, on the subject of biomarkers and lab tests, there are still vast numbers of psychiatric “patients” who have swallowed the psychiatric lie, and who believe that a scan of their brains would reveal the putative pathology.  Why is it that the Director of the NIMH will acknowledge on his blog that no biomarkers or lab tests exist to confirm a psychiatric “illness”, but has taken no steps to enlighten the general public on this matter?  Why is the NIMH not screaming this message from the rooftops, and calling for the censure of those psychiatrists and drug companies who continue to deceive their clients and the public in this way?

“No question, in a field without biomarkers, there is a risk of over-diagnosis. No question, subjective diagnosis could invite unnecessary treatment and over-medication. But what if the increased use of medication reflected more children with severe developmental problems and more families in crisis? What if the bigger problem is not over-medication but under-treatment? Hearing that 7.5 percent of children are on medication (4.2 percent on psychostimulants) seems stunning, but knowing that 11 percent of children have a diagnosis of ADHD raises a possibility of under-treatment.”

Dr. Insel concedes a “risk of over-diagnosis” and the possibility of “unnecessary treatment and over-medication”.  But his terminology is problematic.  “Over-diagnosis” or, for that matter “under-diagnosis”, inevitably implies that there is a correct level of diagnosis.  To take an analogy from general medicine, there is a rare autoimmune disease called Wegener’s granulomatosis.  It is generally acknowledged that this illness is under-diagnosed.  In other words, a certain proportion of people who really have this disease are not so diagnosed during medical examinations. But the point is that the terms under-diagnosis and over-diagnosis only have meaning in reference to something that is reliably definable, a condition which does not apply to psychiatric “illness”.  Psychiatric “illnesses” are nothing more than loose clusters of vaguely defined problems of thinking feeling, and/or behaving.  There is no accurate or real level of diagnosis against which judgments of over-, or under-, diagnosis can be made.

But Dr. Insel makes no attempt to address this question of possible “over-diagnosis” and “over-medication”.  Instead, he goes straight to the heart of psychiatry’s ever-expansionist agenda:  “What if the bigger problem is not over-medication, but under-treatment?”

This, incidentally, is the same Dr. Insel who in April 2013 wrote:

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

 So, although “symptoms alone rarely indicate the best choice of treatment”, here he comes, a year later, expressing concern that only 4.2% of America’s children are taking stimulant drugs, when 11% have “a diagnosis of ADHD.”  The clear implication being, that if a child has this invalid diagnosis, he should be taking the pills.

 “What I hear from families in crisis is lack of access, poor quality care, and a desperate need for answers. In the media reports on over-medicating children, this perspective is missing. The possibility that there is a real increase in the number of children suffering with severe emotional problems, just as there is a real increase in the number of children with diabetes and food allergies, is not even considered. Shouldn’t we be asking why so many children, at younger ages, are being seen for emotional and behavioral problems?”

To which I can only reply:  “Yes, Dr. Insel, we certainly should!”

And we should also be asking why the Director of the NIMH, the nation’s think-tank on mental health matters, is addressing these profound and controversial issues in such misleadingly simplistic terms.

Second Generation Neuroleptics and Acute Kidney Injury in Older Adults

On August 19, 2014, the Annals of Internal Medicine published a paper titled Atypical Antipsychotic Drugs and the Risk for Acute Kidney Injury [AKI] and Other Adverse Outcomes in Older Adults.  The authors were Joseph Hwang et al, and the study was conducted at the Institute for Clinical Evaluative Sciences in Ontario, Canada.  The primary funding source was the Academic Medical Organization of Southwestern Ontario.  The principal investigator was Amit X. Garg, MD, PhD, a kidney specialist at the London Health Science Center and the London Kidney Clinical Research Unit in Ontario, Canada.

Here is the authors’ conclusion:

“Atypical antipsychotic drug use is associated with an increased risk for AKI and other adverse outcomes that may explain the observed association with AKI. The findings support current safety concerns about the use of these drugs in older adults.”

CONTEXT

By way of background, the authors point out that each year  “…millions of older adults worldwide are prescribed atypical antipsychotic drugs (quetiapine, risperidone, and olanzapine),” and that these drugs are  “…frequently used to manage behavioral symptoms of dementia, which is not an approved indication…”

The research is based on a retrospective matched pair cohort study using information drawn from healthcare databases.

METHOD

From the databases, the researchers identified 215,543 Ontario residents who received a new oral antipsychotic prescription for an atypical neuroleptic (quetiapine, risperidone, or olanzapine) between June 2007 and December 2011.  For the same time period they identified 1,726,930 residents who did not receive a new prescription for any of these products.

From these populations, they identified 97,777 neuroleptic drug recipients, and the same number of drug non-recipients, matched on eleven health status factors.  They then checked the matching against 91 measured characteristics.  The authors report that:  “The 2 groups were well-balanced and showed no meaningful differences in the 91 measured baseline characteristics…”  The percentages for the two groups on the 91 characteristics are set out in the report, and the groups are indeed extremely well matched.

RESULTS

The study’s results are presented in Table 1.

Table 1 Garg doc

As can be seen, the risk of acute kidney injury was 1.73 times greater for the drug recipients than for the non-recipients. Also, note that the risk for all-cause mortality was 2.39 times greater for the drug recipients.

There were 3681 “excess” deaths from all causes in the drug group during the 90-day period.  That amounts to 3764 per 100,000 – almost 4%!

Because this was an observational study, as opposed to a randomized, controlled trial, it is not possible to say definitively that the drugs caused the excess kidney failures and deaths.  However, the authors did take great pains to identify and eliminate confounding factors.  For instance, they repeated the analysis for the 180 days preceding the index date, and found no difference in the incidence of AKI in the drug vs. non-drug groups prior to the administration of the neuroleptic drug.  (relative risk 1.02).

The authors also point out that the excess mortality is consistent with the 17 randomized placebo-controlled trials on which the FDA’s 2005 black box warning was based.  These trials showed a 1.6 to 1.7 times greater risk of death associated with neuroleptic use in older people with dementia.  (Average follow-up period:  10 weeks).

It is also noteworthy that although high neuroleptic dose entailed a greater relative risk of kidney damage than a low dose (1.80 vs. 1.73), the difference was slight.  In other words, even low doses were associated with acute kidney injury.

DISCUSSION

On August 19, Medscape ran an article on this study.  The author was Deborah Brauser.  The article recounts the main findings of the study.  Ms. Brauser also apparently interviewed Amit Garg, MD, the principal investigator.  Here are some quotes from the article:

“‘I was actually surprised that this evidence was so robust. We did the study to determine what the association could be, and we clearly saw it,’ said Dr. Garg.”

“Because of this, Dr. Garg said he was surprised that so many patients were still receiving these prescriptions.

‘We looked at almost 100,000 adults in the province of Ontario who received these medications. This shows how commonly they’re used in just a single province, never mind worldwide,’ he said.

The researchers write that current evidence calls for a careful reevaluation of the prescribing of these medications in older adults.”

Also quoted in the Medscape article is Dilip V. Jeste, MD.  Dr. Jeste is an eminent psychiatrist.  He is a past president of both the APA and the American Association for Geriatric Psychiatry.  He was not associated with the present study, but in his interview with Ms. Brauser he referred to an earlier study that he and some colleagues published in the Journal of Clinical Psychiatry in January 2013.

The objectives of that study were:

“To compare longer-term safety and effectiveness of the 4 most commonly used atypical antipsychotics (aripiprazole, olanzapine, quetiapine, and risperidone) in 332 patients, aged > 40 years, having psychosis associated with schizophrenia, mood disorders, posttraumatic stress disorder, or dementia, diagnosed using DSM-IV-TR criteria.”

And the results:

“Overall results suggested a high discontinuation rate (median duration 26 weeks prior to discontinuation), lack of significant improvement in psychopathology, and high cumulative incidence of metabolic syndrome (36.5% in 1 year) and of serious (23.7%) and nonserious (50.8%) adverse events for all atypical antipsychotics in the study.”

And the conclusions:

“Employing a study design that closely mimicked clinical practice, we found a lack of effectiveness and a high incidence of side effects with 4 commonly prescribed atypical antipsychotics across diagnostic groups in patients over age 40, with relatively few differences among the drugs. Caution in the use of these drugs is warranted in middle-aged and older patients.”

I found the last sentence quoted above puzzling.  Given the findings, so clearly stated earlier, why not advocate cease and desist, rather than caution?

And in the Medscape interview, Dr. Jeste spoke very favorably of the current study:

“‘I think this is a really good study…'”

“‘It had a large sample size, and it was interesting how they selected people. They chose only those who were starting on the atypicals, which is appropriate. They also followed them for 90 days and did their best to have a similar control group.'”

But, again, puzzling:

“‘The bottom line is not that people should stop using these medications in older people. However, they should be more cautious, especially in patients with low blood pressure or evidence of kidney injury in the past.'”

There is this enormous reluctance among psychiatrists, even those who clearly have begun to see the light, to take a clear, unambiguous stand against harmful interventions.  So often, they settle for the old face-saving caveat – “use caution”.  But how can one use caution in prescribing a drug for an age group in which it has been shown to lack effectiveness and has a very high incidence of serious adverse effects?    Surely the cautious approach would be not to use these drugs at all, especially since it’s virtually impossible to predict which individuals will suffer AKI or other adverse outcomes, including death.

Even Dr. Garg, principal investigator in the present study, backed off a cease and desist recommendation.

“The current available evidence calls for a careful reevaluation of prescribing atypical antipsychotic drugs in older adults, especially for the unapproved indication of managing behavioral symptoms of dementia…The drugs should be used only after other approaches have been exhausted; when prescribed, patients must be warned about potential adverse effects. Proactive clinical monitoring shortly after initiation seems reasonable (for example, serum creatinine and blood pressure measurement, and if readily available, a bladder scan to detect urinary retention).  When patients present with AKI, atypical antipsychotic drugs should be considered a potential cause and be promptly discontinued if feasible.”

And in his interview with Ms. Brauser:

“‘We wanted to raise awareness around this issue and recommend that physicians should be cautious around the use of these medications in the elderly,’…”

And

“‘However, if a patient is on this medication and the physician is monitoring it very carefully, we don’t want to be alarmists. But it’s healthy to have these types of conversations.'”

ALSO INCIDENTALLY

The incidence of chronic kidney disease (CKD) is increasing among people 65 and over.

Here’s a graph from the National Kidney and Urological Diseases Information Clearinghouse:

 

New CKD casesI’m not suggesting that all of this increase is due to neuroleptics.  However, AKI often progresses to chronic kidney disease, and given the widespread prescribing of these products, it is reasonable to infer that the neuroleptics are a significant contributor.

Here’s a quote from a 2009 editorial of the Clinical Journal of the American Society of Nephrology, The Nexus of Acute Kidney Injury, Chronic Kidney Disease, and World Kidney Day 2009, authors Mark Okusa, MD, et al.

“Acute kidney injury (AKI) is a devastating disease that affects patients throughout the world and is associated with high morbidity and mortality. It has been traditionally thought that patients who do survive recover renal function; however, recent population-based evidence strongly suggests that this may not be the case in many instances. New data suggest that a strikingly large percentage of patients who have AKI require permanent renal replacement therapy or do not fully recover renal function, and that this population has an important and growing impact on the global epidemiology of chronic kidney disease (CKD) and end-stage renal disease (ESRD).”

AND A FINAL NOTE

In 2009, Gwen Olsen published her book Confessions of an Rx Drug Pusher.  In one of the chapters, she described how she systematically, and successfully, targeted nursing homes as markets for neuroleptic drugs.

There is a very poignant passage in which she describes, with considerable remorse and misgivings, how a particular resident – an elderly lady, exuberant and at times feisty – was reduced to a docile, inactive shell of her former self through a neuroleptic prescription.

Ultimately it’s a business.  And it won’t stop until the cost of doing that business exceeds the profits.  The findings of Dr. Garg and Dr. Jeste are helpful, of course  They provide clear and unassailable evidence for what we already know:  that in elderly populations, these drugs are being used as chemical straitjackets to “manage” agitation and aggression, and are killing people in the process.

But it is unlikely that polite calls for “caution” will stem the tide.

 

The Use of Neuroleptic Drugs as Chemical Restraints 

On July 17, I wrote a post on the use of neuroleptic drugs as chemical restraints in nursing homes.  The article generated some comments, one of which touched on some very fundamental issues which, in my view, warrant further discussion.  The comment was from drsusanmolchan and read as follows:

“All drugs can be dangerous toxic chemicals when not used appropriately. While many valid points are made in this article, it’s very one-sided and could be considered biased in that it’s written by a psychologist. I’ve seen many patients and families benefit from their use.

Dr Susan Molchan (psychiatrist who doesn’t ascribe to DSM or Pharma)”

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

“All drugs can be dangerous toxic chemicals when not used appropriately.”

Let’s consider an example of a real medication, prescribed to treat a real illness.  If a person has complete kidney failure, he inevitably becomes anemic, because it is a secretion from the kidneys that triggers the bone marrow to produce red blood cells.  To counteract this problem, nephrologists prescribe EPO, or a more modern substitute (darbepoetin alfa), which compensates for the kidneys’ deficit, and resolves the anemia.  This is a perfect example of a medication correcting a functional pathology within the organism.  Of course, if the nephrologist prescribes too much medication, then the concentration of red cells in the bloodstream will get too high, and the medication can truly be said to be having a toxic effect.

But this is not at all comparable to what happens with psychiatric drugs.  Despite decades of deceptive assurances to the contrary, no psychiatric drug has the effect of correcting a functional or structural pathology within the organism.  In fact, the reverse is the case:  all psychiatric drugs operate by creating a pathological state within the organism.

EPO and darbepoetin alfa can indeed become toxic if administrated in wrong doses – but they are not in and of themselves toxic to the organismAll psychiatric drugs are toxic in and of themselves regardless of dosage.  The so-called therapeutic effect and the toxic effect are one and the same.

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

 “While many valid points are made in this article, it’s very one-sided and could be considered biased in that it’s written by a psychologist.”

Whilst I appreciate the recognition that the article contains “many valid points,” I find myself troubled slightly by the notion that it could be considered biased because “…it’s written by a psychologist.”

My arguments against psychiatry are, and have always been, based on logic and evidence.  Turf is not an issue.  Indeed, I am as critical of psychologists who endorse psychiatry’s spurious philosophy and practices as I am of psychiatry itself, and I am strongly opposed to the extension of prescription authority to psychologists.

I will admit, however, that I am biased!  I am biased towards cogency, critical thinking, honest, impartial research, etc…And I am biased against spurious, simplistic explanations; corruption; and despotic paternalism.  But I am not biased towards psychologists, as such.

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

“I’ve seen many patients and families benefit from their use.”

What Dr. Molchan has written in this one short sentence is the essence of psychiatry’s claim to legitimacy:  the drugs work.

My contention, of course, is that the drugs don’t work, in the sense that any putative short-term benefits are far outweighed by the long-term adverse effects.  I have discussed this matter throughout the website with regards to the various classes of drugs that psychiatry uses, but for now I would like to focus on neuroleptics, which is what my original article was about.

My point was that the neuroleptics were – and are – being used as chemical restraints with people who are agitated, aggressive, or otherwise “difficult to manage.”  The article referred specifically to nursing homes and DD group homes, but it is my general contention that neuroleptics are used in this way in all contexts.  Psychiatrists routinely refer to these drugs as “anti-psychotics,” implying that they target crazy thinking.  This is not only erroneous, it is a blatant lie.  They are neuroleptics in the sense that they “grab hold” of the nervous system and have a marked tranquilizing effect.  In an earlier post, Agitation and Neuroleptics, I drew attention to two experiments in which mental health workers had voluntarily taken neuroleptics in order to assess and describe the effects.  Both studies reported marked drowsiness and sedation as the dominant effect.  Neuroleptic drugs also give rise later to a wide range of devastating adverse effects, including a marked increase in movement and agitation – but that’s a different issue.

My primary contention here is that they are used as restraints, and in many cases this is done without the client’s consent.

Western laws on forcible restraint, both statutory and regulatory, have been developed over centuries, and are still developing.  They vary somewhat from place to place, but in all situations, the restrainer is required to act within the limits of the law, and is subject to judicial review in doubtful cases, and to censure, if it is found that the degree of restraint was excessive.

By medicalizing agitation, aggression, and general “unmanageability,” however, psychiatry has effectively skirted and insulated themselves from the ordinary legal safeguards that differentiate civilized society from police states.

In a civilized society, if a police officer injures a person he is restraining, he will be required to answer for this.  Essentially he will have to show that the degree of restraint he applied was needed to ensure safety.  Obviously there are cases of abuse – but that is the standard.  An officer convicted of using excessive force will face sanctions.

But in the psychiatric context, the pretense is made that the chemical restraint is actually medicine needed to treat an illness.  The resulting damage is ignored, and psychiatrists are almost never held accountable.  On the rare occasion that they are held accountable, it is not to the ordinary legal standards applicable to restraints, but rather to the medical standard of “established practice.”  And these standards are drawn up by psychiatrists themselves.  In this way, they manage to circumvent hundreds of years of common law, by claiming that they are doctors treating an illness, when in fact anybody who has had any experience with the system knows that the drugs are used as restraints.

The fact is that neuroleptic drugs do act as chemical restraints, and that is the main use to which they are put in psychiatric practice.  Given their devastating adverse effects, this ought to be a matter of huge concern.  The people who are forcibly restrained in this way are truly living in a pre-civil rights world.  Their restrainers are not held to the same standard of accountability and responsibility as police officers and others whose jobs require them to use physical restraints on occasion.  This situation is all the more disturbing in that the damage potential with the chemicals is so much greater than with physical restraints.

It is time that we as a society come to terms with the reality that these drugs are not medications in any ordinary sense of the term.  They are chemical restraints with no medical qualities whatsoever.  The travesty of hiding these procedures in the guise of “necessary medical intervention” needs to be exposed and brought to an end.

The Use of Neuroleptic Drugs As Chemical Restraints in Nursing Homes

There’s an interesting article in the July-August 2014 issue of the AARP Bulletin.  It’s called Drug Abuse: Antipsychotics in Nursing Homes, and was written by Jan Goodwin.  AARP is the American Association of Retired Persons.   Jan Goodwin is an investigative journalist whose career, according to Wikipedia, “…has been committed to focusing attention on social justice and human rights…”

The article is essentially a condemnation of the widespread and long-standing practice of using neuroleptic drugs to suppress “difficult” behavior in nursing home residents.

Here are some quotes:

“According to Charlene Harrington, professor of nursing and sociology at the University of California, San Francisco, as many as 1 in 5 patients in the nation’s 15,500 nursing homes are given antipsychotic drugs that are not only unnecessary, but also extremely dangerous for older patients.”

“‘The misuse of antipsychotic drugs as chemical restraints is one of the most common and long-standing, but preventable, practices causing serious harm to nursing home residents today,’ says Toby Edelman, an attorney at the Center for Medicare Advocacy in Washington, D.C.”

“If one drug caused sleeplessness and anxiety, she was given a different medication to counteract those side effects. If yet another drug induced agitation or the urge to constantly move, she was medicated again for that.”

“Antipsychotic drugs are intended for people with severe mental illness, such as patients with schizophrenia or bipolar disorder. As such, they carry the FDA’s black-box warning that they are not intended for frail older people or patients with Alzheimer’s or dementia. In those populations, these drugs can trigger agitation, anxiety, confusion, disorientation and even death. ‘They can dull a patient’s memory, sap their personalities and crush their spirits,’ according to a report from the California Advocates for Nursing Home Reform.”

There’s an implication in this quote that neuroleptic drugs have these adverse effects only on frail older people.  In fact, they have these effects on almost everybody who takes them.

Back to the AARP article:

“And pharmaceutical companies have been aggressively marketing their products as an easy and effective way to control these issues.”

Gwen Olsen’s book Confessions of a Rx Drug Pusher (2009) provides some very compelling insights into this kind of pharma marketing, e.g.:

“It was the end of the third quarter, and I was behind in my sales quota for Haldol…So, I determined the best way to build my Haldol business would be to campaign for the institutionalized patient. These patients were not only encouraged to take the medication; they were actually given the drug. This completely eliminated the compliance issue.”

“I set about scheduling training in-services in the local nursing homes and mental health and mental retardation (MHMR) facilities. I increased my call frequency on physicians whom I knew to have nursing home relationships and directorship responsibilities.” (p 48) [Emphasis added]

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

It is particularly heartening to see an article like Jan Goodwin’s in an established magazine such as AARP Bulletin (readership 37 million +).  It represents a huge advance over the take-your-psychiatric-medication-as-the-doctor-ordered drivel that passes for journalism in most mainstream media outlets.  I commend Jan Goodwin, and hope that we see more material of this sort in the future.

At the same time, however, I was disappointed in that the role of psychiatry in the promotion of these neurotoxic chemicals was not even mentioned.  Responsibility for the problem was laid at the feet of pharma, whose aggressive, irresponsible marketing was unequivocally condemned.

But pharma doesn’t write prescriptions.  And pharma didn’t invent the “illnesses” that legitimize these prescriptions.

For the past sixty years, psychiatry’s primary objective has been to promote the spurious and destructive notion that virtually every human problem is an illness.  Their efforts have been extremely successful, and this false notion today permeates our culture, our language, our political and social institutions, and even our nursing homes.

Using dangerous, toxic chemicals to drug a frail, elderly person into submission is possible because psychiatry has invented and sold the fiction that his agitation, anxiety, and aggression are illnesses, and that the toxic chemicals are medications.  Pharma certainly funded the fraud, but it was psychiatry that conducted the “validating research.”  It was psychiatry that codified and formalized the spurious diagnoses into a manual.  And it is psychiatry that lobbies unremittingly for the acceptance of these “diagnoses” by government entities and by other professions.

And this was not an innocent error.  Psychiatrists invented and promoted their fictitious illnesses and their destructive “treatments” to promote their own aspirations to be seen as a legitimate medical specialty, and to expand their business, their influence, and their prestige.

In this process, they have created a monster that feeds on human life, but they continue to insist, against rapidly mounting evidence, that their “diagnoses” are valid and their “treatments” effective, and have engaged the services of an international PR firm to marginalize their opponents and to sell this travesty to the public, the media, and the political establishment.  Psychiatry is not something that is basically OK, that just needs some minor corrections.  Rather, psychiatry is something fundamentally flawed and rotten: a wrong turning in human history; a blot on humanity’s collective conscience.

Let us hope that we see more articles like this in the mainstream media, and that more investigative journalists like Jan Goodwin will find the motivation and the courage to speak out against this disempowering and destructive edifice whose shadow has for too long been allowed to darken the hopes and aspirations of people of all ages.