Here are a few studies I would pull to raise questions about the common wisdom and effectiveness of our current treatment programs.
Schizophrenia
1. Harrow, Factors involved in outcome and recovery in schizophrenia patients not on antipsychotics medications. A 15-Year Multifollowup-up Study. Journal of Nervous and Mental Disease, 195 (2007): 407-414.
This is the long-term study of 145 patients found that recovery rates for unmedicated schizophrenia patients were 40 percent, versus 5 to 6% for those on drugs, and that internal characteristics such as premorbid functioning, achievements, attitudinal approaches and overall sense of resiliency lead to better outcomes.
2. The NIMH CATIE study was the largest drug comparison trial to date, with 1,493 patients diagnosed solely with schizophrenia, aged 18-65, in 57 U.S. treatment sites. Patients were randomly assigned to receive treatment with one of five anti-psychotic drugs, for up to 18 months: Trilafon, Zyprexa, Risperdal, Seroquel, or Abilify (other agents were allowed as concomitant treatments, but no additional antipsychotics).
74% of the patients were unable to complete an 18 month course of treatment with the new drug.
Duration of "successful" treatment ranged from 3 months (olanzapine = Zyprexa) to 1 month (all other
drugs tested). Drop-out rates for lack of success (inefficacious) or inability to tolerate treatment were as follows: 64% olanzapine, 74% risperidone, 75% perphenazine, 79% ziprasidone, and 82% quetiapine.
The Schizophrenia Story
Most of these studies can be downloaded from madinamerica.com.
I. The Case for Neuroleptics
A. Short-term efficacy in knocking down target symptom psychosis
Cole, The National Institute of Mental Health Psychopharmacology Service Center Collaborative Study Group. Phenothiazine treatment in acute schizophrenia. Arch. Gen. Psychiatry (1964): 10:246-61.
In the early 1960s, the National Institute of Mental Health conducted a nine-hospital trial of 344 newly diagnosed schizophrenia patients, and it reported that at the end of six weeks, 75% of the drug-treated patients were much improved compared to 23% of the placebo patients. This was the trial that established short-term efficacy of the drugs, and is still cited today as the most important trial in that regard.
Adams, “Clorpromazine for Schizophrenia: a Cochrane systematic review of 50 years of randomized controlled trials.” BMC Medicine, vol. 3, 15. (Should be able to get online.)
See discussion section.
This Cochrane group in England has done a big retrospective review of this short-term efficacy. This was in 2005, and they found that 50 trials provided at least some valuable evidence of Thorazine’s efficacy, at least over the short-term. Although they concluded that “reliable evidence about its short-term effects is surprisingly weak,” they nevertheless concluded that for every seven people treated with drug, you get one person who does better in terms of global “improvement” than if no drugs were used. However, this isn’t much, and they said, “even this finding may be an overestimate of the positive and an underestimate of the negative effects of giving chlorpromazine.”
B. Efficacy in preventing relapse.
Gilbert. “Neuroleptic withdrawal in schizophrenic patients.” Arch. Gen. Psychiatry (1995): 52:173-188.
Now once people were on the drugs, researchers needed to figure out if they should be maintained on them, and here too they found evidence for using the drugs.
Here’s how the studies, by and large, were designed. About 40% of schizophrenia patients treated with neuroleptics will respond well to them and remain well for the next year. Th relapse studies were mostly conducted in this group of good responders to the drugs. And what the researchers typically did was divide the responders into two groups: One would stay on the drugs, and the others would have their drugs abruptly withdrawn. And what studies of those kind revealed was that 53% of those abruptly withdrawn from their drugs relapsed within 10 months, versus 16% of those kept on the drugs.
That was the conclusion from a meta-analysis published in 1995, the researchers concluding: “The efficacy of these medications in reducing the risk of psychotic relapse has been well documented.”
C. What’s Missing from This Evidence Base?
a) No long-term outcomes
b) No quality of life data
Stip, Happy birthday neuroleptics! 50 years later: la folie du doute. Eur. Psychiatry (2002): 17(3):115-9.
This is somewhat well recognized. In 2002, a journal called European Psychiatry, ran an editorial in which it posed this question:
“After fifty years of neuroleptic drugs, are we able to answer the following simple questions: Are neuroleptics effective in treating schizophrenia?”
The editorial concluded in this way:
“One thing is certain. If we wish to base psychiatry on evidence-based medicine, we run a genuine risk in taking a closer look at what has long been considered fact.”
II. The Historical Case Against Neuroleptics
Can find all of these on madinamerica.com.
Part A: 1964-1980
1. The first hint of a paradox/the one-year outcomes study.
Schooler, “One year after discharge.” Am. J. Psychiatry (1967): 123:986-95.
A year after the NIMH did that first study, its researchers went back to study how the patients were faring. The researchers found that patients who received placebo “were less likely to be rehospitalized than those who received any of the three active phenothiazines.”
Now here is the first hint of a possible paradox. Perhaps a drug that is effective over the short-term is not over the long-term. But it’s just a hint, and one reason is that there is no control over drug use after release from the hospital. We don’t know how many of placebo patients went on the drugs.
2. The NIMH relapse studies.
Prien, Discontinuation of chemotherapy for chronic schizophrenics. Hosp. Community Psychiatry (1971):22:20-3.
Next, in the late 1960s, the NIMH ran two drug-withdrawal studies. Together, these two studies involved more than 250 patients, and what they found, each time, was that relapse rates rose in correlation with drug dosage. Relapse rates were lowest for those on placebo before drug withdrawal, and highest for those on the highest doses of drugs. The researchers concluded:
"Relapse was found to be significantly related to the dose of the tranquilizing medication the patient was receiving before he was put on placebo--the higher the dose, the greater the probability of relapse."
3. Bockhoven’s comparative outcomes study.
Bockoven, Comparison of two five-year followup studies: 1947-1952 and 1967-1972. Am. J. Psychiatry 1977; 133:32-6.
Now at this time, there was still a wing within psychiatry that believed in psychosocial care. Two leaders in this wing, Sanbourne Bockoven and Harry Solomon from Boston, compared relapse rates treated with a sort of progressive form of social care in the pre-drug era to outcomes in the drug era. Here’s what they found:
Forty-five percent of the patients treated at Boston Psychopathic Hospital in 1947 had not relapsed in the five years following discharge, and 76% were successfully living in the community at the end of that follow-up period.
In contrast, only 31% of patients treated in 1967 with drugs at a Boston community health center remained relapse-free for the next five years, and as a group they were much more "socially dependent"--on welfare, etc.--than those in the 1947 cohort.
4. Three comparative studies.
All of this led to some doubts about the long-term merits of antipsychotic drugs. And so in the 1970s, the NIMH funded three trials that compared long-term outcomes for newly diagnosed patients (for the most part) who were treated initially either in a standard way—with drugs in a hospital setting—or in an experimental way that emphasized psychosocial support and selective use of the drugs. Patients weren’t immediately placed on drugs, and only would be placed on them if couldn’t get better without them.
a) In-house NIMH Study (by William Carpenter)
Carpenter, The treatment of acute schizophrenics without drugs, Am. J. Psychiatry, 1977, 134:14-20.
Only 35% of the non-medicated patients relapsed within a year after discharge, compared to 45% of those treated with medication. The medicated patients also suffered more from depression, blunted emotions, and retarded movements.
b) 1978 Rappaport Study
Rappaport, Are there schizophrenics for whom drugs may be unnecessary or contraindictated. Int. Pharmacopsychiatry (1978): 13:100-11.
In this study, Maurice Rappaport and his colleagues at the University of California, San Francisco randomized 80 young male schizophrenics admitted to Agnews State Hospital to drug and non-drug groups. Results:
The patients in both groups stayed, on average, in the hospital around six weeks. Those receiving medications showed greater symptom reduction during that period.
However, results over the three-year followup were grouped as follows:
Severity-illness scale (1-7) Rehospitalization
Placebo-off (24/41) 1.70 8%
Medication-off (17/39) 2.79 47%
Placebo-on (17/41) 3.54 53%
Medication-on (22/39) 3.51 73%
We see that 58% of those randomized to the non-drug arm did quite well over the long-term. They were markedly less symptomatic and only 2/24 had to rehospitalized in the 3-year followup. This is a picture of people recovering, at least to an extent. This group had by far the best outcomes.
The second-best outcomes were seen in patients who long-term were off drugs.
The worst-outcomes group was drug-in-hospital and drug-out-of hospital. (That of course is our standard of care today.)
Here is what the researchers concluded:
“Our findings suggest that antipsychotic medication is not the treatment of choice, at least for certain patients, if one is interested in long-term clinical improvement . . . many unmedicated-while-in-hospital patients showed greater long-term improvement, less pathology at follow up, fewer rehospitalizations, and better overall functioning in the community than patients who were given chlorpromazine while in the hospital.”
c) The Soteria project
Mathews, A non-neuroleptic treatment for schizophrenia. Schizophrenia Bulletin (1979):5:322-32.
Bola, Treatment of acute psychosis without neuroleptics. Journal of Nervous Mental Disease, (2003):191:219-29.
The second study of this type was conducted by Loren Mosher, and was known as the Soteria Project. Loren was head of schizophrenia studies at NIMH, and so was the nation’s top schizophrenia doctor. What he did was randomize patients either into typical hospital care with drugs, or they would go to a house—the Soteria house—that was staffed by non-professionals. These were people who were just empathetic toward others. There would be massage, yoga, things like that. Idea was that they would be with them in times of crisis.
The findings:
At end of six weeks, no difference in psychopathology scores between two groups
At the end of two years, the Soteria patients as a group had “lower psychopathology scores, fewer (hospital) readmissions, and better global adjustment” than those treated conventionally with drugs in a hospital setting.
In terms of their medication use, only 19% of the patients treated without drugs in Soteria were then eventually placed on drugs and kept on the drugs for two years.
39% of Soteria patients eventually used antipsychotics on a temporary basis.
42% of the Soteria patients were never exposed to neuroleptics during the 2-year study, and this was the group that had the best outcome among the Soteria patients.
5. NIMH Conclusions By Three NIMH leaders in 1970s.
Loren Mosher.
He was head of schizophrenia studies at NIMH, and he believed the Soteria project showed a better way. Should try environmental care with no immediate neuroleptization.
William Carpenter:
Lead researcher at the NIMH facility, and one of the big figures in American psychiatry. He raised this question:
“There is no question that once patients are placed on medication, they are less vulnerable to relapse if maintained on neuroleptics. But what if these patients had never been treated with drugs to begin with? We raise the possibility that antipsychotic medication may make some schizophrenic patients more vulnerable to future relapse than would be the case in the natural course of the illness.”
Jonathan Cole.
Cole, Maintenance antipsychotic therapy. Is the cure worse than the disease? Am. J. Psychiatry (1977): 133:32-6.
He was the director of the Psychopharmacology Service at the NIMH in the 1960s, and had led that first NIMH trial that declared neuroleptics effective over the short term. In 1977, however, he wrote an article titled: “Is the cure worse than the disease.” He made two points:
a) Neuroleptics could cause a great deal of harm over the long-term. A lot of patients maintained on the drugs were developing tardive dyskinesia, which is characterized by a loss of motor control resulting from permanent brain damage.
b) Fifty percent of schizophrenics appeared to be able to do fairly well without the drugs.
Thus, he concluded: “Every chronic schizophrenic outpatient maintained on an antipsychotic medication should have the benefit of an adequate trial without drugs.”
Part B: A Biological Explanation for Drug-Induced Chronicity
In the late 1970s, Canadian investigators at McGill University identified the biological changes induced in the brain by antipsychotic drugs that led to the higher relapse rates. Because the drugs dampen dopamine activity, the brain tries to compensate by becoming “supersensitive” to dopamine. In particular, the drugs trigger an increase in the density of dopamine receptors. This perturbation in dopamine function, over the long term, makes the patients more biologically prone to psychosis and to worse relapses upon drug withdrawal.
Chouinard, Neuroleptic-induced supersensitivity psychosis. Am. J. Psychiatry (1978): 135:1409-1410.
Chouinard, G. Neuroleptic-induced supersensitivity psychosis. Am. J. Psychiatry (1980): 137:16-20.
Chouinard concluded:
“Neuroleptics can produce a dopamine supersensitivity that leads to both dyskinetic and psychotic symptoms. An implication is that the tendency toward psychotic relapse in a patient who has developed such a supersensitivity is determined by more than just the normal course of the illness.”
Part C: Twenty-five Years of Confirming Evidence
Since 1980, there have been a number of long-term outcome studies that confirm the fact that antipsychotic drugs increase the likelihood a person will become chronically ill.
1. The World Health Organization Studies.
Leff, The International Pilot Study of Schizophrenia:five-year followup findings. Psychol. Med (1992):22:131-45.
a) The international pilot study of schizophrenia
Began in 1968
1202 patients in nine countries
Results:
At two-year and five-year follow-ups, the schizophrenia patients in the poor countries "had a considerably better course and outcome than (patients) in developed countries. This remained true whether clinical outcomes, social outcomes, or a combination of the two was considered."
Two-thirds of the patients in India and Nigeria were asymptomatic at the end of five years. The WHO investigators, however, were unable to identify a variable that explained this notable difference in outcomes.
b) The Determinants of Outcome of Severe Mental Disorders
Jablensky, Schizophrenia: manifestations, incidence and course in different cultures. A World Health Organization ten country study. Psychol Med (1992):20 (Monograph suppl):1-95.
In this study, the WHO is looking to explain the findings of the first study.
1379 patients in 10 countries. Majority were first episode and 86% had been ill fewer than 12 months.
Results:
This study confirmed the outcomes of the first study. Two-year outcomes were much better for the patients in the poor countries.
In broad terms, 37 percent of the patients in the poor countries (India, Nigeria and Colombia) had a single psychotic episode and then fully recovered; another 26.7% of the patients in the poor countries had two or more psychotic episodes but still were in "complete remission" at the end of the two years. In other words, 63.7% of the patients in the poor countries were doing fairly well at the end of two years.
In contrast, only 36.9% of the patients in the U.S. and six other developed countries were doing fairly well at the end of two years.
The researchers concluded that "being in a developed country was a strong predictor of not attaining a complete remission."
One variable the WHO investigators looked out as a possible “determinant of outcome” was medication use. They hypothesized that people in the poor countries would be more medication compliant. That greater use of drugs would be the cause of the better outcomes, and that made general sense—drugs are supposed to shift long-term outcomes for the better. However, they found that only 15.9% of patients were continuously maintained on neuroleptics, compared to 61% of patients in the U.S. and other developed countries.
Bottom Line
Outcomes better in countries where drugs are infrequently used.
2. The Vermont Longitudinal Study (reported in 1990)
Harding, The Vermont Longitudinal Study of persons with severe mental illness: Long-Term Outcomes of Subjects Who Retrospectively Met DSM-III Criteria for Schizophrenia. American Journal of Psychiatry 144 (1987):727-734.
Harding, Empirical correction of seven myths about schizophrenia with implications for treatment. Acta Psychiatrica Scand (1994): 90 (suppl. 384):140-6.
Next, we have a long time study conducted by Courtenay Harding, who is now at Boston University. She followed patients released from the back wards of Vermont State Hospital n the 1950s and 1960s. She looked at how they were doing twenty years later.
Results:
Twenty-five to 50% of the patients were completely off their medications, suffered no further signs and symptoms of schizophrenia, and were functioning well. She concluded that it was a “myth” that schizophrenia patients must be on the drugs all their lives, and the reality was that “it may be a small percentage who need medication indefinitely.”
She also noted, in an interview, that all those who had completely covered shared one thing in common: They all had gotten off their drugs.
3. The 1994 Harvard Medical School Retrospective Study on Long-Term Outcomes
Baldessarini, One Hundred Years of Schizophrenia. Meta-Analysis of the Outcomes Literature. American Journal of Psychiatry 151 (1994):1409-1416.
Results:
Outcomes for schizophrenia patients in the U.S. had declined since the 1970s, to the point they were no better than they had been in 1900. Although the researchers did not blame antipsychotics for the poor outcomes, it is notable that this decline occurred during a period when American psychiatrists began telling the public that people diagnosed with schizophrenia had to stay on the drugs for life. In other words, the decline coincided with the adoption of a paradigm of care that emphasized lifelong drug therapy.
4. The MRI Studies
Gur, Subcortical MRI volumes in neuroleptic-naïve and treated patients with schizophrenia. Am. J.. psychiatry 1998; 155; 1711-7.
In the 1990s, researchers ran a number of MRI studies that found that antipsychotic drugs shrink the frontal lobe and increase the size of the basal ganglia. Once they had found this, they wanted to find if these morphological changes correlated with a change in symptoms. As the doctors who conducted these studies remained believers in the antipsychotics, they expected these changes would correlate with an improvement in symptoms. However, in 1998, researchers at the University of Pennsylvania reported that the enlargement of the basal ganglia was associated, over an 18-month period, with a worsening of both the positive and negative symptoms of schizophrenia.
This is a powerful experiment, and it tells an iatrogenic tale. Outside agent comes in, causes change in the brain, and as that occurs, the patient worsens.
5. Progressive Brain Damage
See madinamerica.com for examples of this.
During the 1990s, there were also a number of studies that charted progressive dysfunction in the dopaminergic tracts in the brain associated with continual medication use. Three tracts:
a) basal ganglia and motor movement. Leads to tardive dyskinesia, 5% a year, cumulative.
b) Limbic system. Mount emotional reactions. Tardive psychosis sets in as deteriorates. Best estimate is 3% to 5% a year.
c) Frontal Lobes. Worry about self, self-consciousness, etc. But as the frontal lobes shrink and the dopaminergic tracts become dysfunctional, get cognitive decline and even an inability to monitor self. Something like half of people with severe tardive dyskinesia are unaware of their tardive dyskines.
6. Harrow and Jobe’s 15-year study.
Harrow, Factors involved in outcome and recovery in schizophrenia patients not on antipsychotics medications. A 15-Year Multifollowup-up Study. Journal of Nervous and Mental Disease, 195 (2007): 407-414.
Results:
a) Global Assessment Scale, 1-8, with one best and eight worst.
On Drugs Off Drugs
2.5 year FU 6.17 5.36
4.5 year FU 6.39 3.43
7.5 year FU 5.94 3.47
10 year FU 6.62 3.00
15 year FU 5.67 3.55
b) Active Psychotic Symptoms
On Drugs Off Drugs
10 year FU 79% 23%
15 year FU 64% 28%
c) Recovery Rates
Recovery defined as asymptomatic, no hospitalizations in previous year, pretty good social functioning, and working at least half-time.
On Drugs Off Drugs
2.5 year FU 7% 21%
4.5 6% 39%
7.5 12% 40%
10 6% 44%
15 year 5% 40%
F. The Finnish studies
Seikkula, Five-year experience of first-episode nonaffective psychosis in open-dialogue approach. Treatment principles, follow-up outcomes, and two case studies. Psychotherapy Research 16 (2006):214-228.
Here are the five-year results form Jaako Seikkula:
Outcomes
82% of his schizophrenia or psychotic patients did not have psychotic symptoms, 86% had returned to their studies or were working
14% were on a disability allowance.
Medication use
29% of his patients been exposed to an antipsychotic drug during the five years.
17% were on antipsychotics at the end of five years.
G. Other Treatments Working:
Rogers et al. (1967); May (1968), May et al. (1976, 1981); Grinspoon et al. (1972) & Messier et al. (1969); Paul et al. 1972, Paul & Lentz 1977; Karon & VandenBos (1981); Mosher et al. (1995), Bola & Mosher (2003).
Five of the six studies included long-term data, and three of the above had statistically superior outcomes in the non-drug treatment group. One of the three had superior outcomes with experienced therapists, but results with inexperienced therapists were mixed, suggesting that the quality of the psychosocial program significantly affects the results (Karon & VandenBos, 1981).
Five of the six studies included short-term data. Two found better short-term outcomes in the non-drug group, two had better outcomes in the neuroleptic group, and one had mixed results. Questions about the quality of the therapy in the two studies with negative outcomes raises the possibility that neuroleptics may not even be necessary in the short-term, if appropriate psychosocial interventions are available.
OK, now the bad news:
Neuroleptic Induced Mortality
Joukamaa, M., Heliova, M., Knekt, P. at el, Schizophrenia, neuroleptic medication and mortality, In Bri. J of Psychiatry (2006), 188, P.122-127.
Followed 99 people diagnosed schizophrenic for 17 years. Usage of even one neuroleptic drug increased the risk of dying by 3 fold (35% died). 3 neurleptics increased the risk of dying in 17 years by 7 fold! (57% died)
1 NL at baseline 35% died
2 NLs 44% died
3 NLs 57% died
Relative risks of mortality for the schizophrenics, relative to normal healthy controls:
zero NL at baseline 1.29
1 NL 2.97
2 NL 3.21
3 NL 6.83
Healy, D. Harris, M. at el. (2006) Lifetime suicide rates in treated schizophrenia: 1875-1924 and 1994-1998, In Brit J. of Psych, 18, 8, p. 223-228. http://bjp.rcpsych.org/cgi/content/abstract/188/3/223
*This is the largest study EVER done to address suicide in schizophrenia patients.
* The widely cited lifetime rate of 10% for suicide in patients with schizophrenia is incorrect for both the pre- and post-community care eras.
* The best estimate for the life time rate of suicide in patients with schizophrenia in the pre-community care era is of the order of 1% or less.
* Although de-institutionalism is probably the single most important factor in determining suicide rates in patients with schizophrenia, pharmacotherapy appears to contribute to this risk, and is the element of current care that is undermost clinical control.
This represents at 20 FOLD INCREASE in suicide rates for patients treated in modern period.
Diekman, A., and Whitaker, L. (1979). "Humanizing the Psychotherapy ward: Changing
from drugs to psychotherapy." Psychotherapy: Theory, Research, and Practice. 16
(2):204-214.
This 11 month study compared typical hospital treatment with pure psychological treatment, noting the most severe cases went to the psychological treatment without medication. Results were no suicide attempts, elopements or other significant acts of violence in the psycho-social treatment group; however, typical hospital drug group with a higher staffed ward had 3 suicides.
BUT AREN'T THOSE DIAGNOSED DANGEROUS?
Danger to Others?
Crawford, M., 2000, Homicide is Impossible to Predict, Psychiatric Bulletin 24: 152.
Professor Mike Crawford states there are no instruments that can accurately identify people at high risk for committing violent incidents, and that for every one person correctly identified, 5,000 people might be incorrectly identified (false positive) as high risk for homicide.
In general= Not Violent
The 1988 Department of Justice study found that only 4.3% of all homicides in a sample of the nation's 33 largest counties had been committed by assailants with a history of mental illness. This did not limit the criteria to "schizophrenia".
Dawson, J.M. and Langan, P.A. (1994). 1988 Department of Justice study. Retrieved May 18, 2006 at: http://www.psychlaws.org/BriefingPapers/BP11.htm
Ten years later, a Washington State evaluation of more than 300 mentally ill offenders released from prison found that only 2% committed serious violent crimes in the first 18 months of a scheduled 5 year follow-up.
Kisely, S., Campbell, L.A., and Preston, N. (2005). Compulsory community and involuntary outpatient treatment for people with severe mental disorders [abstract]. Cochrane Database Systematic Reviews, Jul 20 (3): CD004408. and
and
Lovell, D., Gagliardi, G.J., and Phipps, P. (2005). Washington's Mentally Ill Offender Law: Was Community Safety Increased? Retrieved May 18, 2006 at: http://depts.washington.edu/washinst/One%20Page%20Summaries/Mentally%20Ill%20Offender%20Studi es.htm
The fact is, the severely mentally ill are usually prey, not predators. Published in 2005, the results of a large study conducted by researchers at Northwestern University examined rates of criminal victimization. After interviewing 936 patients in the Chicago area, the investigators found that people diagnosed with severe mental illness were 6 to 23 times more likely to be victims of violent crime than the general population.
Teplin, L.A. (1985). The criminality of the mentally ill: a dangerous misconception [abstract]. American Journal of Psychiatry, 142, 593-9.
Teplin, L.A., Abram, K.M., and McClelland, G.M. (1994). Does psychiatric disorder predict violent crime among released jail detainees? A six-year longitudinal study. American Psychologist, 49, 335-342.
Teplin, L.A., McClelland, G.M., Abram, K.M., and Weiner, D.A. (2005). Crime Victimization in Adults With Severe Mental Illness: Comparison With the National Crime Victimization Survey. Archives of General Psychiatry, 62, 911-921.
Over ninety percent (90%) “of persons with mental illness have no history of violence….through media sensationalism (it sells papers) the cases that do occur stand out in peoples minds.” Serper, M, Bergman, A. (2003) Psychotic Violence: Methods, Motives, Madness, Psychosocial Press of Madison, CT.
Those Who Are Violent= Dual Dx, Substance Abuse, Freq Moving, Younger, Aggression prior to Dx, Stopping Rx abruptly
The GREATER risk of violence is from those who have dual diagnosis, i.e., individuals who have a mental disorder as well as a substance abuse disorder.
Swanson, 1994;
Eronen et al, 1998;
Steadman et al., 1998.
Monahan, J. and Shah, S. Dangerousness and commitment of the mentally disordered in the United States. Schizophrenia Bulletin, 15: 541-553. Reprinted in: Social and Clinical Psychiatry, 1991, 1: 56-70 [in Russian].
Found people Dx Sz and Bipolar were no more violent than general population, unless problems with substance abuse or psychopathology.
Cirincione, C., Steadman, H., Robbins, P. and Monahan, J. Schizophrenia as a contingent risk factor for criminal violence. International Journal of Law and Psychiatry 15: 347-358.
Walsh E, Buchanan A, Fahy T., Br J Psychiatry. 2002, Violence and schizophrenia: examining the evidence. Jun;180:490-5. full text: http://bjp.rcpsych.org/cgi/content/full/180/6/490 Section of Forensic Mental Health, Institute of Psychiatry, Denmark Hill, London. sppmemw@iop.kcl.ac.uk
The proportion of societal violence attributable to schizophrenia is small.
METHOD: A review of population-based studies on the epidemiology of violence and schizophrenia. Population-attributable risks for violence in schizophrenia were calculated.
RESULTS: Recent good evidence supports a small but independent association. Comorbid substance abuse considerably increases this risk. The proportion of violent crime by people Diagnosed with schizophrenia falls below 10%. CONCLUSIONS: Strategies aimed at reducing this small risk require further attention, in particular treatment for substance misuse.
Swanson, J. and Swartz, M., The British Journal of Psychiatry (2008) 193: 37-43. Comparison of antipsychotic medication effects on reducing violence in people with schizophrenia.
This study of 1,445 Sz randomly assigned to 1 of 5 Rx groups. Violence declined with from 16% to 9% with the group maintained on drugs the whole time, and from 19% to 14% with the group who did not stay on the medications the whole time (e.g. intent to treat, Thus Both Groups had Violence Reduced, but just more with Rx compliance. BUT NO Difference with people diagnosed schizophrenic with antisocial behaviors. Confounding variable was the stopping of drug caused the aggression. No Rx free control was used as a comparison group.
Brekke JS, Prindle C, Bae SW, Long JD, Risks for individuals with schizophrenia who are living in the community. Psychiatr Serv. 2001 Oct;52(10):1358-66. http://ps.psychiatryonline.org/cgi/content/full/52/10/1358 School of Social Work, University of Southern California, Los Angeles, CA 90089-0411, USA. brekke@usc.edu
This study examined incidence and predictors of police contact, criminal charges, and victimization for people Dx schizophrenic & schzioaffective. N=172, in urban LA between 1989-1991. 6 month follow ups over 3 year period. R/O=sub abuse
RESULTS: 48% had contact police contact (victim or perpetrator). A small percentage of the contacts involved aggressive behavior against property or persons. Being younger, more address changes at baseline, and having a history of arrest and assault were significant predictors. 22% had charges filed against them so some reason or another, not necessarily aggression. Poorer social functioning, more address changes, fewer days of taking medication at baseline, and a history of arrest and assault were significant predictors of criminal charges. 38% reported having been the victim of a crime during the three years, 91% of which was violent. Having more severe clinical symptoms and more substance use at baseline were significant predictors of victimization. 14 times more likely to be victims of a violent crime than to be arrested for one.
Arseneault L, Moffitt TE, Caspi A, Taylor PJ, Silva PA. Mental disorders and violence in a total birth cohort: results from the Dunedin Study. Arch Gen Psychiatry. 2000 Oct;57(10):979-86.
Institute of Psychiatry, 111 Denmark Hill, London SE5 8AF, England.
Report on mental disorders and violence for 94% of a total-city birth cohort in New Zealand, April 1, 1972, through March 31, 1973. Researchers looked in 1999 of those born in 1972-1973 and looked at violence for the prior year (i.e. measured by self-reports of offending and a search of official conviction records). Variables accounted. for: Substance use before violence, adolescent excessive perceptions of threat, and a juvenile conduct disorder, mental disorders and violence.
RESULTS: only 10% of violence risk was uniquely attributable to schizophrenia-spectrum disorder), by excessive perceptions of threat and a history of conduct disorder.
Violence and Delusions: Data from the MacArthur Violence Risk Assessment Study, by Applebaum P, Robbins P, and Monahan J. Am J Psychiatry 2000; 157:566-572.
This follow-on to the MacArthur study, which found that recently discharged psychiatric patients were not more dangerous than people in the communities they were discharged to, finds that those same patients were not more dangerous even if they had threat/control delusions. "...[T]he presumed risk of violence associated with delusions per se does not justify hospitalization of a patient...."
Anti-psychotics may not lower aggression.
Rabkin, J.1979, Criminal Behavior of Discharged Mental Patients, Psychological Bullentin, 86, 1-27. Patients discharged prior to 1955, neuroleptic drugs, committed crimes equal to or less than general population, but then in 1965 and 1979, post neuroleptic adminstration, patients discharged intoxicated were being arrested at rates exceeding those of general population.
Tyrer P, et al "Risperidone, haloperidol, and placebo in the treatment of aggressive challenging behavior in patients with intellectual disability: a randomized controlled trial" Lancet 2008; 371: 57-63.
The trial included 86 nonpsychotic patients with an IQ of less than 75 who presented with aggressive challenging behavior at 10 centers in England and Wales and one in Australia. Although aggression decreased substantially whether patients were given a typical or an atypical antipsychotic, the greatest improvements were seen with placebo (65%, 58%, and 79% from baseline, P=0.06), reported Peter Tyrer, M.D., of Imperial College
Pro re nata or PRN’s (“as needed” Rx) may not lower aggression either.
Rosack, J, PRN Orders May Benefit Staff More Than Patients, In Psychiatric News, vol XXXVIII no 19, Oct 3, 2003 p35-36
The original Study published in Sept., 2003, Psychiatric Services, and funded by the Stanley Foundation and National Institutes of Health. PRN’s are nurse ordered drugs to prevent or limit agitation, anxiety, and physical aggression. Arkansas State Hospital in Little Rock Nov. 1, 1999 through February, 2000 banned PRN orders for psychotropic medications, and needed to rely upon “order medications” from a doctor. Dr. Thapa stated, “we were able to look at the frequency of unscheduled (doctor) orders prior to the change and compare that with the frequency after the policy shift… (and)…what we found was clearly a dramatic reduction in the use of unscheduled psychotropic medications-greater than a 40 percent reduction."
Thapa and his colleagues examined the frequency of nonscheduled psychotropic medication use before the policy change (both PRN and "now" orders) and while the ban was in effect (only "now" orders). "The underlying concern at the time-among the psychiatrists and the staff-was that the delay caused by having to contact one of the
physicians for a 'now' order might result in patients getting a bit out of hand or too agitated," Thapa said. "The concern was that it would result in an increase in the use of seclusion and restraint for incidents of aggression."
Unexpected Results Raise Questions
Thapa and his colleagues were able to collect data retrospectively on medication orders, as well as the use of seclusion and restraint and any events involving aggression on the part of patients.
"We did not see any increase in adverse events when staff lost the
option of PRN orders," Thapa explained. In fact, the team found an
interesting trend in the use of seclusion and restraint, although the
number of times they were used during each period studied was low,
making it impossible to reach statistical significance.
"In terms of just numbers, though,"
Thapa said, "the use of seclusion and restraint actually decreased."
During the period when PRN orders were not allowed-resulting in the 47
percent reduction in unscheduled medication orders-the number of times
seclusion was utilized to manage patient behavior decreased from 48
events to 41 events, and the use of restraints was cut in half, from
eight to four times.
"Clearly this was reassuring," Thapa continued, "but essentially, then,
one could argue whether the PRN orders are really necessary." In fact,
Thapa and his colleagues wrote, "The results of our study thus raise the
uncomfortable question of whether PRN orders are for the benefit of the
patient or the staff."
Thapa noted several limitations in the study. At Arkansas State
Hospital, staff psychiatrists are in the hospital 24 hours a day, seven
days a week. This makes obtaining a "now" order relatively easy and
quick for the staff. On units where a psychiatrist must be paged or
called to get an order, the increased amount of time necessary to do so
becomes a significant variable.
"What we really need to think about is that in selected patients, with
certain circumstances, having the ability to write PRN orders would be
beneficial for the staff and helpful for the patient," Thapa told
Psychiatric News. "But by not really thinking about it-with no controls
or restrictions on PRN orders-we just kind of reflexively throw in a PRN
order or two-perhaps whether the patient needs it or not. We really need
to evaluate this and, if PRN orders are to be used, then I think they
should be used very judiciously."
Many hospitals across the country, he noted, have attached restrictions
to PRN orders-for example, time limits that cause all PRN orders to
expire in three days unless re-evaluated and reordered by the physician.
In addition, some institutions now look for appropriateness of PRN
orders for specific patient conditions.
Thapa and his coauthors believe that "given the objective of regulatory
bodies to minimize the use of 'chemical restraints' in this population
of vulnerable patients, these findings have important policy
implications."
The article, "PRN (As-Needed) Orders and Exposure of Psychiatric
Inpatients to Unnecessary Psychotropic Medications," is posted on the
Web at
http://psychservices.psychiatryonline.org/cgi/content/full/54/9/1282.
Psychiatr Serv 2003 54 1282
SO WHAT MIGHT CAUSE SOMEONE TO DEVELOP PSYCHOSIS?
Psychological – Social- Cultural Factors
in the Development of Schizophrenia...JUST A FEW!
Social Factors- General
Wicks et al (2005-"Social adversity in childhood and the risk of
developing psychosis: a national cohort study" American Journal of
Psychiatry; 162:1652-1657), studied 2.1 million persons born in Sweden
from 1963-1983 to investigate the relationship between social adversity in
childhood and later risk of developing psychosis. They concluded: "...this
national population-based cohort study of two generations showed increased
risks for schizophrenia and other psychoses in children from
less-advantaged households, thus indicating that social adversity in
childhood or fetal life contributes to the risk of developing
schizophrenia" (p.1656).
In a recent review of the relevant research, Jane Boydell, Jim van Os and
Robin Murray (2004), in their "Is there a role for social factors in a
comprehensive developmental model for schizophrenia?" (contained in an
excellent new volume "Neurodevelopment and Schizophrenia" edited by
Matcheri Keshavan, James Kennedy and Robin Murray in 2004 for Cambridge
University Press), noted:
"In the 1950's and 1960's, there was much extravagant discussion of the
role of social factors in the etiology of schizophrenia. However, there
was little scientific basis to this speculation, and it was swept away by
the demonstration that people with schizophrenia showed abnormalities of
brain structure on computed tomographic scans (Johnstone et al 1976) [it
soon became apparent to those of us who were studying both areas of
neuroscience research, schizophrenia and the effects of profound
fear/stress/anxiety/trauma/social isolation on CNS structure/function,
that there was a substantial overlap between the two areas of scientific
inquiry]. A decade later, the neurodevelopmental model of schizophrenia
was proposed, and it subsequently became the dominant etiological and
pathogenetic model (Murray and Fearon, 1999; Murray et al., 1992). As a
result of these two developments, researchers have come to regard
schizophrenia as a brain disease, and social factors have been largely
ignored as putative etiological agents.
It is increasingly clear, however, that the neurodevelopmental model, an
essentially neurological concept, does not explain all the available data
about schizophrenia. One consequence has been a revival during the 1990's,
particularly in Europe, of research into the role of social factors as
causal agents in schizophrenia" (p.224).
Boydell et al (2004) pointed to the neurobiological effects of isolation
rearing and social stress in animals. For example, rats raised in
isolation demonstrated structural and physiological differences from
controls in the hippocampi. Isolation raised rats demonstrate anxiety,
learning deficits (analogue of working memory, hypofrontality, etc.?),
sensory changes, dopaminergic dysfunction, etc (see the excellent research
of Myron Hofer on the psychobiology of developmental loss and separation).
In terms of human development, social relationship experiences may alter
prefrontal neural systems which mediate emotional self-regulation (Lyons
et al 2002). The early social environment impacts on various levels of
psychobiological and neurobiological development. The early social
environment has been demonstrated to induce synaptic changes that may be
indicative of, and perhaps the cause of, alterations in behavioral and
cognitive functioning (Ovtscharoff and Braun 2001).
There is evidence that the early social environment can mediate the establishment of neural
networks that regulate a child's response to stress and emotional
self-control (DiPietro 2000).
Boydell et al (2004) have identified the following broad categories in
which social factors have been implicated in the initiation and course of
the schizophrenias: family factors (mother-child relationship,
unwantedness, family communication deviance, dysfunctional family
environment, communal upbringing, early parental loss, expressed emotion,
childhood abuse, etc.); an urban effect (city birth, city upbringing,
etc.); social isolation (during childhood, moving schools in adolescence,
in young adult life, at time of onset, migration and ethnic minority
status, discrimination, unemployment, etc.); life events (socioeconomic
factors, deprivation, inequality, etc.); interaction between social and
other etiological factors (gene-environment interaction,social factors and
cognitive processing, social causation versus social selection, etc.).I
shall summarize the main research findings in each category.
Family Factors
Mother-child relationship
The British 1946 cohort study followed all children born in 1 week, a
total of 5,362 subjects. By age 43, there were 30 cases of schizophrenia.
One of the most powerful risk factors for later schizophrenia, was the
quality of the mother-child relationship at age 4, as rated by health
visitors. A poor relationship (e.g., rated as less understanding-perhaps
in line with the research constructs of Fonagy and colleagues, e.g.,
'mentalization,' and its relevance to borderline phenomena) carried a
sixfold increase in risk for later schizophrenia.
Similarly, the Dunedinstudy which followed 1000 children from birth to age 26 with comprehensive medical and psychiatric assessments, demonstrated that the mothers of
children who developed schizophreniform disorders were rated as having
poorer attitudes and behavior towards their children at age 3. The British
1946 and the Dunedin studies are particularly interesting since they are
population-based, as opposed to high-risk studies. However, is the
increased risk a function of impaired caregiving or is impaired caregiving
a function of a genetic diathesis in the parent or a reaction to a
disturbed child.? Some research studies have suggested that impaired
relatedness is an independent variable which accounts for the variance
apart from the latter two variables (i.e., parental genetic diathesis
and/or parental reaction to a disturbed child).
Unwantedness
Myrhrman et al (1996) used the Northern Finland 1966 Birth Cohort (11,017
individuals) followed through age 28. When mothers were 6 or 7 months
pregnant, they were asked by a midwife if their pregnancies were wanted,
mistimed but wanted, or unwanted. The risk of developing schizophrenia was
considerably raised for the unwanted children even after adjusting for
sociodemographic, pregnancy (including depression), and perinatal
variables.
Family Communication deviance
A study by Wahlberg et al (1997, 2000) found a significant interaction
between high genetic risk for schizophrenia (i.e., having a biological
mother diagnosed with schizophrenia) and communication deviance in the
adoptive parents. The high risk but not the control adoptees showed
greater evidence of thought disorder if their adoptive parents showed
communication deviance. This demonstrates genetic control of sensitivity
to the environment or environmental control of gene expression.
Dysfunctional family environment
In the Finnish Adoptive Family Study by Tienari and colleagues the risk
of developing a schizophrenia spectrum disorder was higher in those
adopted-away offspring of schizophrenic parents who were exposed to a
dysfunctional adoptive family-rearing environment. The most recent data
from this study suggests that the adopted-away offspring may have lower
risk than children who remain with their parent with schizophrenia.
Similarly, the Danish-American adoption studies suggested that the
high-risk adopted-away offspring had a lower chance of developing
schizophrenia than those who remained with their biological parents
(Rosenthal et al 1971), suggesting the importance of the caregiving
environment as neuroprotective.
Communal upbringing
In the Israeli High Risk Study (Mirsky et al 1985), 46 children with high
genetic risk, half of whom were raised communally on a kibbutz (where
their parents lived) and half in family homes, were compared with
controls. High risk children were significantly more likely to develop a
schizophrenic or affective disorder if they were raised communally as
opposed to being raised in a family home. Similar results were observed in
the Copenhagen High Risk Project (public care institutions as opposed to a
kibbutz).
Early parental loss
Agid et al (1999) observed a significant correlation between parental
loss before the age of 8, particularly loss of the mother through death,
and development of schizophrenia.
Similarly, Mallett et al (2002) found that separation from both parents in childhood discriminated UK African-Caribbean individuals with schizophrenia from Afro-Caribbean
controls.
Expressed emotion
Social over stimulation and high-expressed emotion are associated with
relapse in schizophrenia, a finding that has been replicated many times
over. This does not have to refer only to family settings, but can be
extended to other social situations, e.g., inpatient wards.
Childhood abuse
Many researchers have documented a correlation between childhood traumas
(sexual, physical and emotional abuse) and later psychosis (Read et al
2001). In a recent study, childhood abuse was a significant predictor of
hallucinations, even in the absence of adult abuse (Read et al 2003).
Patients with a diagnosis of bipolar disorder and PTSD who also report a
history of childhood abuse have a high frequency of delusions and
hallucinations. It has been suggested that, of all diagnostic categories,
psychosis displays the strongest associations with childhood abuse.
Boydell et al (2004) noted: "The experience of abuse may create a
biological (Read et al 2001) or psychological (Garety et al 2001)
vulnerability for the development of psychotic symptoms, including
subclinical psychotic experiences such as low-grade delusional ideation
and isolated auditory hallucinations (Johns and van Os 2001)" (p.229).
In both clinical and non-clinical populations (Ross and Joshi 1992), the
diagnostic group with the highest rate of of childhood abuse consistently
reported the most Schneiderian symptoms (first rank symptoms of
schizophrenia).
One difficulty with the above studies is that they are cross-sectional in
nature and have a potential bias in terms of self-report. In a recent
three year longitudinal study of a general population sample of 4,045
subjects from age 18-64 with no previous psychotic symptoms, baseline
reported childhood abuse predicted development of clinically relevant
positive psychotic symptoms associated with need for care (Janssen et al
2004). This association remained even after adjusting for a range of risk
factors and demographic variables.
The cornerstone of Read's tectonic plate-shifting evidence is the 40 studies
that reveal childhood or adulthood sexual or physical abuse in the history of
the majority of psychiatric patients (see, also, Read's book, Models of
Madness). A review of 13 studies of schizophrenics found rates varying from 51% at
the lowest to 97% at the highest. Crucially, psychiatric patients or schizophrenics who report abuse are much more likely to experience hallucinations. The content of these often relate directly to the trauma suffered.
The urban effect
City birth
Arguing against the prevalence of the 'downward-drift' theories, many
studies have shown strong effects for urban birth and/or urban upbringing.
One of the most impressive was conducted by Mortensen et al (1999) with a
Danish population-based cohort of 1.75 million subjects. There were strong
effects for urban birth. There was a clear dose-response relationship for
urbanicity in that the larger the town of birth, the greater the risk of
development of a psychotic disorder. A family history of schizophrenia did
not explain or effect the results. The investigators calculated a 34.6%
population attributable fraction for urban birth compared with 9% and 7%
respectively, for having a mother or father with schizophrenia.
City upbringing
Pedersen and Mortensen (2001) used a comprehensive Danish national
registration system that accurately recorded changes in residence to
demonstrate that risk of developing schizophrenia increased with the
number of years that an individual lived in an urban area and with an
increasing degree of urbanization.
Social drift and social residue theories
The social drift hypothesis cannot explain the results of the above
research studies. In addition, Dauncey et al (1993) investigated where
patients lived 5 years prior to their first hospital admission in
Nottingham, UK and were unable to find support for systematic geographic
drift. In the Danish study by Mortensen et al (1999), the investigators
ruled out downward drift as a viable explanation for urban excess. A
family history of schizophrenia did not explain or effect the urban-rural
difference in the Mortensen or other studies (van Os et al 2002). This is
also relevant for the social residue theory (that those at greater risk
are 'left behind' in an area as it becomes less desirable because they do
not have the resources to move out).
Possible explanations
Possible etiologic factors hypothesized to explain urban excess have
been: infectious agents, lead pollution, and social factors (e.g., social
isolation, deprivation, and adverse life events). Boydell et al (2004)
noted:
"...while there is no direct evidence that the urban excess is caused by
social factors, the fact that its effect is so widespread across the
population is compatible with the notion that part of the excess risk
represents a psychological reaction to factors in the wider social
environment. certainly some of the major differences between urban and
rural areas are to do with social cohesion and support" (p.231).
Social factors can, with some vulnerable individuals, act in concert with
genetic risk.
Social Isolation
During childhood
Many clinicians from Bleuler onwards have noted that individuals who
develop schizophrenia have had relatively solitary backgrounds including
fewer social networks (parenthetically, severity of symptomatology is
correlated with size of social network and I am aware of one neuroimaging
study which correlated atrophic neural regions with size of social
network) and friends. The British 1946 cohort study (Jones et al 1994)
observed that preference for solitary play at age 4 or 6 was associated
with later schizophrenia. In addition, self-reported anxiety at age 13 and
teacher-rated anxiety at age 15 both showed linear associations with later
risk for developing schizophrenia.
Moving schools in adolescence
A research finding emerging from the Danish study of Pedersen and
Mortensen (2001) was that change in municipality and therefore school,
increased the risk for later schizophrenia but not change of address
within the municipality. Geographic moves during the early teen years had
the greatest risk and the more moves, the greater the risk factor (this
was a finding I observed in my patients at a long-term state psychiatric
hospital-I theorized that these changes and uprootings created
discontinuities in the self leading to a lack of cohesion of the self).
In young adult life
The Swedish conscript study also looked at the role of premorbid
personality for later development in 50087 individuals. The investigators
found that there was a significantly increased risk of later developing
schizophrenia in young men who
felt they were more sensitive than theirpeers,
had fewer than two close friends,
preferred small groups, and
did not have a girl friend. Once again, Boydell et al (2004) raised the
possibility of a gene-environment interaction: "Until proven otherwise, it
is wise to consider that both may be true: individuals with a schizoid or
schizotypal personality may be less able to make social relationships, and
then the social isolation may propel them further toward frank psychosis"
(pp.232-233).
At time of onset
Hare (1956) observed that social isolation, as measured by proportion of
single person households in a geographic area, was associated with higher
rates of schizophrenia. This finding was not accounted for by downward
drift. One theory is that disruption of social networks decreases a
person's capacity to cope with psychosocial stress and may increase the
risk for developing schizophrenia.
Van Os et al (2000) demonstrated that single people had a slightly higher
risk of developing psychosis if they lived in a neighborhood with fewer
single persons compared with a neighborhood with many other single people
(theoretically, this would increase the person's sense of social
exclusion, loneliness and isolation).
Jablensky and Cole (1997) demonstrated that marriage had a protective effect and that this was not simply a function of better adjusted males being able to marry.
Migration and etnic minority status
As early as 1932, Odegard (1932) observed that Norwegian persons
migrating to the USA had an increased risk of developing psychosis. It was
thought that the cultural and geographic disruption resulted in paranoia
and alienation. This is a robust finding (i.e., migration as a risk factor
for psychosis) and has been demonstrated amongst many migrant groups
(Castle et al 1991;Harrison et al 1988, 1997; King et al 1994; Selten et
al 1998, 2001; van Os et al 1996;etc). Research methodological issues such
as 'category fallacy' (cultural variation in diagnosis), misdiagnosis,
inaccurate estimation of the denominator, etc., have been overcome in
studies which still demonstrate an excess of psychosis in migrant groups
even when moving to similar cultures (Bruxner et al 1997). Even when
controlling for urbanicity (i.e., excess urban effect-since many migrants
settle in urban areas), studies demonstrate an excess migration effect
(van Os et al 2001).
Elizabeth Cantor-Graee, Krystyna Zolkowska, and Thomas McNeil
(2005-"Increased risk of psychotic disorder among immigrants in Malmö; a
3-year first-contact study" Psychological Medicine, 35, 1155-1163)
examined the risk of first contact for psychotic and schizophrenic
disorders among first- and second-generation immigrants to risks in native
'Swedes.' The results were that first-generation immigrants, not
second-generation immigrants, to Sweden had an increased risk of
developing psychotic and schizophrenic disorders compared to Swedes. The
effect was greater in first-generation immigrants with 'black' skin color
and for those born in a developing country.
African-Caribbeans in the UK
Much research has investigated the increased rates of psychosis in the
African-Caribbean population in the UK and the Netherlands. Genetic
diathesis cannot be the sole explanation since the increased risk is not
shared by the population of origin in the Caribbean (Bhugra et al 1997;
Mahy et al 1999). In addition, the risk for second-generation siblings is
much greater than for their first-generation equivalents (Hutchinson et al
1996; Sugarman and Crawford 1994). Selective migration has been ruled out
in a Surinamese population which migrated to the Netherlands (Selten et al
2002). Other variables which have been ruled out include
neurodevelopmental insults secondary to obstetric complications and viral
infections, as well as the role of substance misuse (McGuire et al 1995;
Selten et al 1997).
Morgan et al (2005) studying the African-Caribbean population in the UK
sought to explain whether social isolation is a risk factor for psychosis
and whether this might partially account for the high rates of psychosis
among this population in the UK. They observed that a number of indicators
of social isolation, such as having no close confidants or relationships
and unemployment, were associated with risk of developing psychosis. They
found strong evidence that the risk of psychosis increased as levels of
social isolation increased. An index of social isolation demonstrated a
strong dose-response relationship with development of psychosis. Whether
this association is correlational or causal is not straightforward,
however, the data are suggestive of a causal role of social isolation in
the later development of psychosis.
The second generation
There are many studies demonstrating higher rates of schizophrenia in the
children of migrants. This has been observed in Greenland (Mortensen et al
1999), in the USA (Malzberg 1969), and in the UK with the Afro-Caribbean
population (Harrison et al 1988). In the Yemenite Jewish population which
migrated to Israel, Weingarten and Orren (1983) observed a high prevalence
of schizophrenia among the offspring (the adults did not integrate into
Israeli society and their lifestyle was considered primitive). Since the
entire population migrated to Israel, selective migration cannot account
for the findings.
Boydell et al (2004) concluded:
"There is no satisfactory explanation as to why there are higher rates of
psychosis in children of migrants, but the range of countries and
circumstances in which this phenomena has been described is suggestive of
a socially induced phenomena" (p.235).
Discrimination
Psychosis has also been attributed to such factors as racism (overt and
institutionalized), social isolation, and reduced social networks. Boydell
et al (2001) demonstrated that incidence rates of schizophrenia increased
in ethnic minorities as the proportion of ethnic minorities in the
locality fell, suggesting that social experience (isolation,
discrimination, etc.) contributed to development of the illness. Janssen
et al (2003) measured subjective experiences of discrimination and
subsequent development of psychotic illness 3 years afterwards. Experience
of discrimination strongly predicted for the development of delusional
ideation. Janssen et al (2002) also demonstrated that the effect of ethnic
minority status on psychosis was no longer significant when controlling
for the experience of discrimination. Karlsen and Nazroo (2002) studied
the experience of ethnic harassment and discrimination among a UK
representative sample of 5000 persons from ethnic minorities. They
demonstrated significantly increased OR (odds ratio) for a range of health
problems and particularly psychosis. Mallett et al (1998) demonstrated
that one of the main distinguishing characteristics of first-onset
patients of Caribbean origin with psychosis in London was that they lived
alone and also had been separated from their mothers at an early age.
Racism
Karlsen et al (2005-"Racism, psychosis and common mental disorder among
ethnic minority groups in England" Psychological Medicine, 35, 1795-1803)
concluded from their research in the UK, that experiences of interpersonal
racism and perceiving racism in the wider society each have independent
effects on the risk of developing a psychotic disorder, after controlling
for gender, age, and socio-economic status.
Unemployment
Bhugra et al (1997) observed high unemployment in persons of Caribbean
origin first presenting with schizophrenia in the UK. An analogous effect
was not observed in Tinidad (Bhugra et al 2000). Perhaps the social milieu
in Trinidad is more tolerant of those at risk of developing schizophrenia
and that there is greater stigmatization in London.
Stress- Excess Life events
Brown and Birley (1968) observed an excess of life events three weeks
prior to an episode of schizophrenia. Prospective studies have also
demonstrated an association between life events and relapse into psychosis
(Malla et al 1990; Ventura et al 1989). Bebbington (2000), using a
case-control study in London, found a significant excess of life events in
the three months prior to onset of schizophrenia (I believe similar
research findings have been documented in affective illness-perhaps the
model of Post et al on 'kindling' is relevant here-we see more life events
earlier in the onset and progression of the disease than in later
episodes-theoretically, because later episodes do not require as much
stimulation to cross threshold into active psychosis). There is evidence
that it is not so much major life events that precipitate psychotic
relapse in vulnerable individuals, but what psychoanalysts call
narcissistic injuries of one kind or another encountered in daily life.
Part of this sensitivity may be rooted in exposure to earlier major life
events (Myrin-Germays et al 2003), suggesting "synergistic
environment-environment interactions" (Boydell et al 2004, p. 237).
Boydell et al (2004) speculated that:
"Stress may be generated in part by underlying personality traits, whose
genetic contribution may overlap with that of schizophrenia.
Alternatively, individuals with vulnerability to schizophrenia may be more
sensitive to the effects of stress, while sensitivity to stress is also
determined by the degree of prior exposure to stress, possibly including
stress in early life (Janssen et al 2004)" (p. 237).
Socioeconomic factors, deprivation, and inequality
Several research studies have found a relation between economic
deprivation and incidence rates of psychosis, prevalence and admission
rates of schizophrenia (Croudace 2000). Recent studies have implicated
inequality as a risk factor. Boydell et al (2003) found a positive
correlation between incidence rates of schizophrenia and degree of
inequality in deprived areas in London, after adjusting for such variables
as age, sex, absolute deprivation and ethnicity.
Social defeat
Selten and Cantor-Graae (2005) proposed that long-term exposure to social
defeat, defined as a subordinate position or outsider status, leads to
disturbed dopamine (DA) functions in the brain (there is research
indicating that the mesolimbic DA system in persons with schizophrenia is
sensitized) and places the individual at risk for developing a
schizophrenic disorder.
Social fragmentation
Allardyce et al (2005-"Social fragmentation, deprivation and urbanicity:
relation to first-admission rates for psychoes" The British Journal of
Psychiatry 187: 401-406) concluded from their research in Scotland, that
first-admission rates for the psychoses were strongly associated with
measures of social fragmentation, independent of material deprivation and
the urban/rural etiologic factor.
Social Selection Belief System:
OK, SO NOW YOU NEED HELP EXPLAINING THIS TO SOMEONE ELSE...LIKE A JUDGE OR A LAWYER....I CAN HELP.
AFFIDAVIT OF DR. TOBY T. WATSON, Psy.D.
STATE OF ________________ )
) ss. DISTRICT COURT
COUNTY OF )
I. Personal Background
1. I have been the Clinical and Doctoral Training Director of Associated Psychological Health Services, Inc., in Sheboygan, WI, for over six years, full service outpatient mental health treatment center for nearly thirty years, specializing at treating individuals severely suffering with psychological problems often diagnosed as Schizophrenic, Schizo-Affective, Bipolar and severely depressed. I am also the past International Executive Director of the International Society for Ethical Psychology and Psychiatry, a professional 501-C non profit research and educational organization, founded almost 40 years ago and comprised of over 300 psychiatrists, psychologists, social workers, professors and teachers, researchers, attorneys and lay individuals, and am currently the Chief Supervising Psychologist for the State of WI- Kettle Moraine Correctional Institution. I have supervised psychologists, social workers, interns, externs and master level therapists, as well as I have been a weekly consultant to psychiatrists and psychologists through several professional organizations and other treatment centers across the United States, and I have testified as a psychological expert both on behalf for the State, as well as defendants.
2. I am a Licensed Clinical Psychologist in the State of Wisconsin, having earned a Doctorate in Clinical Psychology, Psy.D., by Alliant University in Fresno, CA, AND
my Psy.D. training was specifically created in 1969 to allow doctors to focus their expertise upon the abundance of research produced by the more academic and research minded Ph.D. individuals in order to integrate and apply the research into the clinical practice. Thus, my formal training and expertise is in understanding peer reviewed research and development data, then translating and applying that research into the clinical practice. In summary, I am here to testify to optimal treatment plans based on the evidence and peer reviewed psychiatric research.
3. I have completed the following specialized research-practice orientated training; however, acknowledge this is only a limited account of my training:
a. Two years of clinical training at Sequoia Psychotherapy Center, formally San Joaquin Psychotherapy Center, in Fresno CA, a non medical model Day Treatment Milieu, specializing at treating people diagnosed with Schizophrenia,
b. One year of Clinical Psychology Internship, One year of Post-Doctoral Clinical Training, and a third year of treating patients while under supervision at Allendale Association-Bradley Counseling Center, in Lake Villa, IL, again working with patients often diagnosed with Schizophrenia, Bipolar and severely depressed,
c. Individualized Continuing Education training and daily consultation through the International Society for Ethical Psychology and Psychiatry (ISEPP), for approximately nine years, and six consecutive years at the International Society for the Psychological Treatments of Schizophrenia and other Psychosis (ISPS).
d. No less than 15 hours per year by accredited Continuing Educational Seminars specifically focusing upon the areas treatment indicated above.
4. I have been lecturing at professional conferences upon the biological model of mental illness (e.g. Genetic Studies, Chemical Imbalance Studies, Family, Twin and Adoption Studies, and Functional and Structural Brain Scan Studies), and upon outcome data related to psychotropic medication interventions for the past seven years. I have presented Continuing Legal Educational Units at the American University Washington Collage of Law in Washington, D.C. in conjunction with ISEPP (formerly ICSPP), specifically upon the research and outcome data used in Involuntary Forced Medication Commitments. I am also professional Member of National Alliance of Professional Psychologist Providers (NAPPP), ISPS, the National Coalition of Mental Health Professionals and Consumers (NCMHP), and I am listed with the National Register of Psychologists.
5. I have been specifically researching the effects of psychotropic medication on outcomes, and how the use of such drugs may help or hinder positive outcomes for over a decade. I wish to highlight some of the research work of colleague Robert Whitaker.
Mr. Whitaker from 1989 to 1994 was the science and medical writer for the Albany Times Union in Albany, New York; was from 1992-1993 a fellow in the Knight Fellowship for Science Writers at the Massachusetts Institute of Technology; was from 1994-1995 the director of publications at Harvard Medical School; co-founded a publishing company in 1994, CenterWatch, that reported on the clinical development of new drugs; and was the recipient of several national awards, including the George Polk Award for medical writing in 1999, the National Association of Science Writers award for best magazine article, and most notably was a finalist for the Pulitzer Price in Public Service in 1999, when he wrote in the Boston Globe upon problems in psychiatric research. Since 1999, Mr. Whitaker has focused upon writing books, such as Mad in America, a report on our country’s treatment of the mentally ill throughout its history whereby he explored in particular why schizophrenia patients fare so much worse in the United States and other developed countries than in the poor countries. This first book was picked by Discover magazine as one of the best science books of 2002 and the American Library Association named it as one of the best histories of 2002.
6. Prior to researching upon the effects of psychotropic medications in therapy, I shared conventional beliefs about the nature of schizophrenia and the need for patients so diagnosed to be on antipsychotic medications, sometimes for life, to maintain and gain competency and positive outcomes. I had been trained by experts in psychopharmacology, neurology and psychophysiology, experts who told me that the drugs were like “insulin for diabetes” and corrected a chemical imbalance in the brain.
7. However, I came upon two studies that looked at long-term outcomes for schizophrenia patients that raised questions about this model of care. First, in 1994, Harvard researchers reported that outcomes for schizophrenia patients in the United States had declined in the past 20 years and were now no better than they had been in 1900.[1] Second, the World Health Organization twice found that schizophrenia patients in the poor countries of the world fare much better than in the U.S. and other “developed” countries, so much so that they concluded that living in a developed country was a “strong predictor” that a person so diagnosed would never recover.[2],[3] Although the WHO didn’t identify a reason for that disparity in outcomes, it did note a difference in the use of antipsychotic medications between the two groups. In the poor countries, only 16% of patients were regularly maintained on antipsychotic medications, whereas in the U.S. and other rich countries, this was the standard of care, with 61% of schizophrenia patients staying on the drugs continuously. (Exhibit 1)
II. Overview of Research Literature on Schizophrenia and Standard Antipsychotic Medications
8. Although the public has often been told that people with schizophrenia suffer from too much “dopamine” in the brain, researchers who investigated this hypothesis during the 1970s and 1980s were unable to find evidence that people so diagnosed have, in fact, overactive dopamine systems[4]. In fact, attempts to quantify D2 receptor density in vivo with PET scans have also proved inconclusive results.4 Within the psychiatric research community, this was widely acknowledged in the late 1980s and early 1990s. As Pierre Deniker, who was one of the founding fathers of psychopharmacology, confessed in 1990: “The dopaminergic theory of schizophrenia retains little credibility for psychiatrists.”[5]
9. Since people with schizophrenia have no known “chemical imbalance” in the brain, antipsychotic drugs cannot be said to work by “balancing” brain chemistry. These drugs are not like “insulin for diabetes.” They do not serve as a corrective to a known biological abnormality. Instead, Thorazine and other standard antipsychotics (also known as neuroleptics) work by powerfully blocking dopamine transmission in the brain. Specifically, these drugs block 70% to 90% of a particular group of dopamine receptors known as D2 receptors.[6] This thwarting of normal dopamine transmission is what causes the drugs to be so problematic in terms of their side effects.
10. Psychiatry’s belief in the necessity of using the drugs on a continual basis stems from two types of studies.
a) First, research by the NIMH has shown that the drugs are more effective than placebo in curbing psychotic symptoms over the short term (six weeks).[7],[8]
b) Second, researchers have found that if patients abruptly quit taking antipsychotic medications, they are at high risk of relapsing. [9]
11. Although the studies cited above provide a rationale for continual drug use, there is a long line of evidence in the research literature, one that is not generally known by the public or even by most psychiatrists, that shows that these drugs, over time, produce these results:
a) They increase the likelihood that a person will become chronically ill.
b) They cause a host of debilitating side effects.
c) They lead to early death.
III. Evidence Revealing Increased Chronicity of Psychotic Symptoms
12. In the early 1960s, the NIMH conducted a six-week study of 344 patients at nine hospitals that documented the efficacy of antipsychotics in knocking down psychosis over a short term. (See footnote five, above). The drug-treated patients fared better than the placebo patients over the short term. However, when the NIMH investigators followed up on the patients one year later, they found, much to their surprise, that it was the drug-treated patients who were more likely to have relapsed/ This was the first evidence of a paradox: Drugs that were effective in curbing psychosis over the short term were making patients more likely to become psychotic over the long term.[10]
13. In the 1970s, the NIMH conducted three studies that compared antipsychotic treatment with “environmental” care that minimized use of the drugs. In each instance, patients treated without drugs did better over the long term than those treated in a conventional manner.[11], [12], [13] Those findings led NIMH scientist William Carpenter to conclude that “antipsychotic medication may make some schizophrenic patients more vulnerable to future relapse than would be the case in the natural course of the illness.”
14. In the 1970s, two physicians at McGill University, Guy Chouinard and Barry Jones, offered a biological explanation for why this is so. The brain responds to neuroleptics and their blocking of dopamine receptors as though they are a pathological insult. To compensate, dopaminergic brain cells increase the density of their D2 receptors by 40% or more. The brain is now “supersensitive” to dopamine, and as a result, the person has become more biologically vulnerable to psychosis than he or she would be naturally. The two Canadian researchers wrote: “Neuroleptics can produce a dopamine supersensitivity that leads to both dyskinetic and psychotic symptoms. An implication is that the tendency toward psychotic relapse in a patient who had developed such a supersensitivity is determined by more than just the normal course of the illness. [14]
15. MRI-imaging studies have powerfully confirmed this hypothesis. During the 1990s, several research teams reported that antipsychotic drugs cause atrophy of the cerebral cortex and an enlargement of the basal ganglia.[15], [16], [17] In 1998, investigators at the University of Pennsylvania reported that the drug-induced enlargement of the basal ganglia is “associated with greater severity of both negative and positive symptoms.” In other words, they found that the drugs cause morphological changes in the brain that are associated with a worsening of the very symptoms the drugs are supposed to alleviate.[18]
IV. Research Showing that Recovery Rates are Higher for Non-Medicated Patients than for Medicated Patients (i.e. they tend to have better functioning and competency).
16. The studies cited above show that the drugs increase the chronicity of psychotic symptoms over the long term. There are also now a number of studies documenting that long-term recovery rates are much higher for patients off antipsychotic medications. Specifically:
a) In 1994, Courtenay Harding at Boston University reported on the long-term outcomes of 82 chronic schizophrenics discharged from Vermont State Hospital in the late 1950s. She found that one-third of this cohort had recovered completely, and that all who did shared one characteristic: They had all stopped taking antipsychotic medication. The notion that schizophrenics needed to stay on antipsychotics all their lives was a “myth,” Harding said.[19], [20], [21]
b) In the World Health Organization studies, 63% of patients in the poor countries had good outcomes, and only one-third became chronically ill. In the U.S. countries and other developed countries, only 37% of patients had good outcomes, and the remaining patients did not fare so well. In the undeveloped countries, only 16% of patients were regularly maintained on antipsychotics, versus 61% of patients in the developed countries.
c) In response to this body of literature, physicians in Switzerland, Sweden and Finland have developed programs that involve minimizing use of antipsychotic drugs, and they are reporting much better results than what we see in the United States.[22], [23], [24], [25] In particular, Jaako Seikkula recently reported that five years after initial diagnosis, 82% of his psychotic patients are symptom-free, 86% have returned to their jobs or to school, and only 14% of his patients are on antipsychotic medications.[26]
d) Then just a few years ago in 2007 researchers at the University of Illinois Medical School reported on the long-term outcomes of schizophrenia patients in the Chicago area since 1990. They found that 40% of those who refused to take their antipsychotic medications were recovered at five-year and 15-year followup exams, versus five percent of the medicated patients.[27]
V. Harmful Side Effects from Antipsychotic Medications
17. In addition to making patients chronically ill, standard antipsychotics cause a wide range of debilitating side effects. Specifically:
a) Tardive dyskinesia. The most visible sign of tardive dyskinesia is a rhythmic movement of the tongue, which is the result of permanent damage to the basal ganglia, which controls motor movement. People suffering from tardive dyskinesia may have trouble walking, sitting still, eating, and speaking. In addition, people with tardive dyskinesia show accelerated cognitive decline. NIMH researcher George Crane said that tardive dyskinesia resembles “in every respect known neurological diseases, such as Huntington’s disease, dystonia musculorum deformans, and postencephalitic brain damage.”[28] Tardive dyskinesia appears in five percent of patients treated with standard neuroleptics in one year, with the percentage so afflicted increasing an additional five percent with each additional year of exposure.
b) Akathisia. This is an inner restlessness and anxiety that many patients describe as the worst sort of torment. This side effect has been linked to assaultive, murderous behavior.[29], [30], [31], [32], [33]
c) Emotional impairment. Many patients describe feeling like “zombies” on the drugs. In 1979, UCLA psychiatrist Theodore van Putten reported that most patients on antipsychotics were spending their lives in “virtual solitude, either staring vacantly at television, or wandering aimlessly around the neighborhood, sometimes stopping for a nap on a lawn or a park bench . . . they are bland, passive, lack initiative, have blunted affect, make short, laconic replies to direct questions, and do not volunteer symptoms . . . there is a lack not only of interaction and initiative, but of any activity whatsoever.[34] The quality of life on conventional neuroleptics, researchers agreed, is “very poor.” [35]
d) Cognitive impairment. Various studies have found that neuroleptics reduce one’s capacity to learn and retain information. As Duke University scientist Richard Keefe said in 1999, these drugs may “actually prevent adequate learning effects and worsen motor skills, memory function, and executive abilities, such as problem solving and performance assessment.”[36]
d) Other side effects of standard neuroleptics include an increased incidence of blindness, fatal blood clots, arrhythmia, heat stroke, swollen breasts, leaking breasts, obesity, sexual dysfunction, skin rashes and seizures, and early death.[37], [38], [39] Schizophrenia patients now commit suicide at 20 times the rate they did prior to the use of neuroleptics.[40]
VI. The Research Literature on Atypical Antipsychotics
18. The conventional wisdom today is that the “atypical” antipsychotics that have been brought to market—Risperdal, Zyprexa, and Seroquel, to name three—are much better and safer than Haldol, Thorazine and the other older drugs. However, it is now clear that the new drugs have no such advantage, and there is even evidence suggesting that they are worse than the old ones.
19. Risperdal, which is manufactured by Janssen, was approved in 1994. Although it was hailed in the press as a “breakthrough “medication, the FDA, in its review of the clinical trial data, concluded that there was no evidence that this drug was better or safer than Haldol (haloperidol.) The FDA told Janssen: “We would consider any advertisement or promotion labeling for RISPERDAL false, misleading, or lacking fair balance under section 501 (a) and 502 (n) of the ACT if there is presentation of data that conveys the impression that risperidone is superior to haloperidol or any other marketed antipsychotic drug product with regard to safety or effectiveness.”[41]
20. After Risperdal (risperidone) was approved, physicians who weren’t funded by Janssen were able were able to conduct independent studies of the drug. They concluded that risperidone, in comparison to Haldol, caused a higher incidence of Parkinsonian symptoms; that it was more likely to stir akathisia; and that many patients had to quit taking the drug because it didn’t knock down their psychotic symptoms.[42], [43], [44], [45], [46] Jeffrey Mattes, director of the Psychopharmacology Research Association, concluded in 1997: “It is possible, based on the available studies, that risperidone is not as effective as standard neuroleptics for typical positive symptoms.”[47] Letters also poured into medical journals linking risperidone to neuroleptic malignant syndrome, tardive dyskinesia, tardive dystonia, liver toxicity, mania, and an unusual disorder of the mouth called “rabbit syndrome.”
21. Zyprexa, which is manufactured by Eli Lilly, was approved by the FDA in 1996. This drug, the public was told, worked in a more “comprehensive” manner than either risperidone or haloperidol, and was much “safer and more effective” than the standard neuroleptics. However, the FDA, in its review of the trial data for Zyprexa, noted that Eli Lilly had designed its studies in ways that were “biased against haloperidol.” In fact, 20 of the 2500 patients treated with Zyprexa in the trials died. Twenty-two percent of the Zyprexa patients suffered a “serious” adverse event, compared to 18 percent of the Haldol patients. There was also evidence that Zyprexa caused some sort of metabolic dysfunction, as patients gained nearly a pound per week. Other problems that showed up in Zyprexa patients included Parkinsonian symptoms, akathisia, dystonia, hypotension, constipation, tachycardia, seizures, liver abnormalities, white blood cell disorders, and diabetic complications. Moreover, two-thirds of the Zyprexa patients were unable to complete the trials either because the drugs didn’t work or because of intolerable side effects.[48]
22. There is now increasing recognition in scientific circles that the atypical antipsychotics are no better than the old drugs, and may in fact be worse. Specifically:
a) In 2000, a team of English researchers led by John Geddes at the University of Oxford reviewed results from 52 studies, involving 12,649 patients. They concluded: “There is no clear evidence that atypicals are more effective or are better tolerated than conventional antipsychotics.” The English researchers noted that Janssen, Eli Lilly and other manufacturers of atypicals had used various ruses in their clinical trials to make their new drugs look better than the old ones. In particular, the drug companies had used “excessive doses of the comparator drug.”[49]
b) In 2005, a National Institute of Mental Health study found that that were “no significant differences” between the old drugs and the atypicals in terms of their efficacy or how well patients tolerated them. Seventy-five percent of the 1432 patients in the study were unable to stay on antipsychotics owing to the drugs’ “inefficacy or intolerable side effects,” or for other reasons.[50]
c) In 2007, a study by the British government found that schizophrenia patients had better “quality of life” on the old drugs than on the new ones.[51] This finding was quite startling given that researchers had previously determined that patients medicated with the old drugs had a “very poor” quality of life.
23. There is also growing evidence that the atypicals may be exacerbating the problem of early death. Although the atypicals may not clamp down on dopamine transmission quite as powerfully as the old standard neuroleptics, they also block a number of other neurotransmitter systems, most notably serotonin and glutamate. As a result, they may cause a broader range of physical ailments, with diabetes and metabolic dysfunction particularly common for patients treated with Zyprexa. In a 2003 study of Irish patients, 25 of 72 patients (35%) died over a period of 7.5 years, leading the researchers to conclude that the risk of death for schizophrenics had “doubled” since the introduction of the atypical antipsychotics. [52]
VII. Subjective Diagnosis and Limitations to Psychiatric Diagnosis
24. Psychological and psychiatric diagnosis are unlike any true medical diagnosis, in that they are phenomenological concepts. When diagnosing a patient, they are given a diagnostic label for simply doing or not doing a particular behavior or having a particular feeling. Thus, this is not unlike being labeled Catholic or socialist. If one goes to mass, says prayers, goes to confession, believes in God and takes communion, then they may be labeled Catholic. They can not “Have” Catholic though. Thus, if a person is anxious, extremely worried, paranoid, hears voices or inner thoughts talking to himself, does not care for his hygiene or becomes overly involved in details, they may labeled with Schizophrenia; however, they can not actually “Have” Schizophrenia, as there is no biological basis, test, or physical matter to distinguish between someone presenting schizophrenic and someone who does not.
Thus, psychiatric diagnosis are subjective and often invalid, allowing for different doctors often come up with several different diagnosis when looking at the same individual. This was notably pointed out by one of the most respected researchers on Schizophrenia, Dr. Nancy Andreasen, citing “although creating standardized diagnoses that would facilitate research was a major goal, DSM diagnoses are not useful for research because of their lack of validity.”[53] The Diagnostic Statistical Manual of Mental Disorders-4th Edition (DSM-IV), the book of all diagnosis and labels for mental health problems, produced by the American Psychiatric Association, states the causes of such symptoms are unknown, and they make no recommendation as to how to treat a person’s suffering.
VIII. The Research Literature on Commitments- Forced Orders.
25. There are few studies meeting a basic minimum validity criteria that have attempted to determine the effectiveness of outpatient commitment orders (OPC). In a thorough review of empirical studies supporting OPC, Dr. Kathleen Maloy concluded "almost no valid empirical evidence in support of the effectiveness of involuntary outpatient commitment vis-a-vis treatment compliance, success in the community for people with severe and persistent mental illness, or amelioration of the problems associated with 'revolving door' patients."[54] The most recent studies addressing the effectiveness were sought out. In 2005, Drs. Kirsley and Campbell, were highlighted by the Cochrane Database of Systematic Reviews, the gold-standard of peer reviewed psychiatric/psychological research, for their research upon the number of outpatient commitment orders (OPC) it takes to prevent one re-hospitalization. They concluded it takes 85 OPC orders to prevent one readmission, 27 to prevent one episode of homelessness and 238 to prevent a future arrest.[55] Thus, 84 people would need to be subjected to a non-required forced treatment program in order to reduce just one re-hospitalization. This lead researchers in 2007, at the Institute of Psychiatry in Maudsley, UK, to conduct “the most comprehensive and through review of outpatient commitments.” They concluded “it is not possible to state whether or community treatment orders (CTOs) [the equivalent to OPC] are beneficial or harmful to patients.”[56]
25. In summary, the research literature reveals the following:
a) Antipsychotics increase the likelihood that a person will become chronically ill.
b) Long-term recovery rates are much higher for unmedicated patients than for those who are maintained on antipsychotic drugs.
c) Antipsychotics cause a host of debilitating physical, emotional and cognitive side effects, and lead to early and premature death.
d) The new “atypical” antipsychotics are not better than the old ones in terms of their safety and tolerability, and quality of life may even be worse on the new drugs than on the old ones.
e) Being diagnosed with any psychiatric disorder, such as Schizophrenia, does not indicate there is a biological disease or true medical illness, and it does not indicate that a person suffering needs to be medicated with psychiatric medications to maintain safety and recover.
f) Forced Commitment Orders have yet to be proven an effective means to reducing re-hospitalizations, and thus, have yet to be determined if they are truly helpful or harmful to patients long term recovery and success.
DATED this ___ day of __________________, 2011, in Sheboygan, WI.
________________________________
Dr. Toby T. Watson, Psy.D.
SUBSCRIBED AND SWORN TO before me this ____ day of ______________, 2011.
________________________________
Notary Public in and for Wisconsin
My Commission Expires:___________
[1] Hegarty, J, et al. “One hundred years of schizophrenia: a meta-analysis of the outcome literature.” American Journal of Psychiatry 151 (1994):1409-16.
[2] Leff, J, et al. “The international pilot study of schizophrenia: five-year follow-up findings.” Psychological Medicine 22 (1992):131-45.
[3] Jablensky, A, et al. “Schizophrenia: manifestations, incidence and course in different cultures, a World Health Organization ten-country study.” Psychological Medicine 20, monograph supplement, (1992):1-95.
[4] Knable, M. B., Kleinman, J. E., & Weinberger, D. R. (1998). Neurobiology of schizophrenia. In A. F. Schatzberg & C. B. Nemeroff (Eds.), Textbook of Psychopharmacology, 2nd ed., (pp.595-596). Washington, DC: American Psychiatric Press.
[5] Deniker, P. “The neuroleptics: a historical survey.” Acta Psychiatrica Scandinavica 82, supplement 358 (1990):83-87.
[6] Wysong, P., PET Brain Scans Best to Determine Schizophrenics’ drug dosages, In Washington Post, April 12, 2000, Vol. 36, Issue 14.
[7] Cole, J, et al. “Phenothiazine treatment in acute schizophrenia.” Archives of General Psychiatry 10 (1964):246-61.
[8] Adams, “Clorpromazine for Schizophrenia: A Cochrane systematic review of 50 years of randomized controlled trails.” BMC Medicine, Vol. 3, 15.
[9] Gilbert, P, et al. “Neuroleptic withdrawal in schizophrenic patients.” Archives of General Psychiatry 52 (1995):173-188.
[10] Schooler, N, et al. “One year after discharge: community adjustment of schizophrenic patients.” American Journal of Psychiatry 123 (1967):986-95.
[11] Rappaport, M, et al. “Are there schizophrenics for whom drugs may be unnecessary or contraindicated?” Int Pharmacopsychiatry 13 (1978):100-11.
[12] Carpenter, W, et al. “The treatment of acute schizophrenia without drugs.” American Journal of Psychiatry 134 (1977):14-20.
[13] Bola J, et al. “Treatment of acute psychosis without neuroleptics: two-year outcomes from the Soteria project.” Journal of Nervous Mental Disease 191 (2003):219-29.
[14] Chouinard, G, et al. “Neuroleptic-induced supersensitivity psychosis.” American Journal of Psychiatry 135 (1978):1409-10. Also see Chouinard, G, et al. “Neuroleptic-induced supersensitivity psychosis: clinical and pharmacologic characteristics.” American Journal of Psychiatry 137(1980):16-20.
[15] Gur, R, et al. “A follow-up magnetic resonance imaging study of schizophrenia.” Archives of General Psychiatry 55 (1998):142-152.
[16] Chakos M, et al. “Increase in caudate nuclei volumes of first-episode schizophrenic patients taking antipsychotic drugs.” American Journal of Psychiatry 151 (1994):1430-6.
[17] Madsen A, et al. “Neuroleptics in progressive structural brain abnormalities in psychiatric illness.” The Lancet 352 (1998): 784-5.
[18] Gur, R, et al. “Subcortical MRI volumes in neuroleptic-naive and treated patients with schizophrenia.” American Journal of Psychiatry 155 (1998):1711-17.
[19] Harding, C. “The Vermont longitudinal study of persons with severe mental illness,” American Journal of Psychiatry 144 (1987):727-34.
[20] Harding, C. “Empirical correction of seven myths about schizophrenia with implications for treatment.” Acta Psychiatrica Scandinavica 90, suppl. 384 (1994):140-6.
[21] McGuire, P. “New hope for people with schizophrenia,” APA Monitor 31 (February 2000).
[22] Ciompi, L, et al. “The pilot project Soteria Berne.” British Journal of Psychiatry 161, supplement 18 (1992):145-53.
[23] Cullberg J. “Integrating psychosocial therapy and low dose medical treatment in a total material of first-episode psychotic patients compared to treatment as usual.” Medical Archives 53 (199):167-70.
[24] Cullberg J. “One-year outcome in first episode psychosis patients in the Swedish Parachute Project. Acta Psychiatrica Scandinavica 106 (2002):276-85.
[25] Lehtinen V, et al. “Two-year outcome in first-episode psychosis according to an integrated model. European Psychiatry 15 (2000):312-320.
[26] Seikkula J, et al. Five-year experience of first-episode nonaffective psychosis in open-dialogue approach. Psychotherapy Research 16/2 (2006): 214-228.
[27] Harrow M, et al. “Factors involved in outcome and recovery in schizophrenia patients not on antipsychotic medications.” Journal of Nervous and Mental Disease 195 (2007): 406-414.
[28] Crane, G. “Clinical psychopharmacology in its 20th year,” Science 181 (1973):124-128. Also see American Psychiatric Association, Tardive Dyskinesia: A Task Force Report (1992).
[29] Shear, K et al. “Suicide associated with akathisia and deport fluphenazine treatment,” Journal of Clinical Psychopharmacology 3 (1982):235-6.
[30] Van Putten, T. “Behavioral toxicity of antipsychotic drugs.” Journal of Clinical Psychiatry 48 (1987):13-19.
[31] Van Putten, T. “The many faces of akathisia,” Comprehensive Psychiatry 16 91975):43-46.
[32] Herrera, J. “High-potency neuroleptics and violence in schizophrenia,” Journal of Nervous and Mental Disease 176 (1988):558-561.
[33] Galynker, I. “Akathisia as violence.” Journal of Clinical Psychiatry 58 (1997):16-24.
[34] Van Putten, T. “The board and care home.” Hospital and Community Psychiatry 30 (1979):461-464.
[35] Weiden P. “Atypical antipsychotic drugs and long-term outcome in schizophrenia.” Journal of Clinical Psychiatry 57, supplement 11 (1996):53-60.
[36] Keefe, R. “Do novel antipsychotics improve cognition?” Psychiatric Annals 29 (1999):623-629.
[37] Arana, G. “An overview of side effects caused by typical antipsychotics.” Journal of Clinical Psychiatry 61, supplement 8 (2000):5-13.
[38] Waddington, J. “Mortality in schizophrenia.” British Journal of Psychiatry 173 (1998):325-329.
[39] Joukamaa, M, et al. Schizophrenia, neuroleptic medication and mortality. British Journal of Psychiatry 188 (2006):122-127.
[40] Healy, D et al. “Lifetime suicide rates in treated schizophrenia.” British Journal of Psychiatry 188 (2006):223-228.
[41] FDA approval letter from Robert Temple to Janssen Research Foundation, December 21, 1993.
[42] Rosebush, P. “Neurologic side effects in neuroleptic-naïve patients treated with haloperidol or risperidone.” Neurology 52 (1999):782-785.
[43] Knable, M. “Extrapyramidal side effects with risperidone and haloperidol at comparable D2 receptor levels.” Psychiatry Research: Neuroimaging Section 75 (1997):91-101.
[44] Sweeney, J. “Adverse effects of risperidone on eye movement activity.” Neuropsychopharmacology 16 (1997):217-228.
[45] Carter, C. “Risperidone use in a teaching hospital during its first year after market approval.” Psychopharmacology Bulletin 31 (1995):719-725.
[46] Binder, R. “A naturalistic study of clinical use of risperidone.” Psychiatric Services 49 (1998):524-6.
[47] Mattes, J. “Risperidone: How good is the evidence for efficacy?” Schizophrenia Bulletin 23 (1997):155-161.
[48] See Whitaker, R. Mad in America. New York: Perseus Press (2002):279-281.
[49] Geddes, J. “Atypical antipsychotics in the treatment of schizophrenia.” British Medical Journal 321 (2000):1371-76.
[50] Lieberman, J, et al. “Effectiveness of antipsychotic drugs in patients with schizophrenia.” New England Journal of Medicine 353 (2005):1209-1233.
[51] Davies, L, et al. “Cost-effectiveness of first- v. second-generation antipsychotic drugs.” The British Journal of Psychiatry 191 (2007):14-22.
[52] Morgan, M, et al. “Prospective analysis of premature morbidity in schizophrenia in relation to health service engagement." Psychiatry Research 117 (2003):127-35.
[53] Andreasen, N. (2007). DSM and the Death of Phenomenology in America: An Example of Unintended Consequences, In Schizophrenia Bulletin vol. 33 no. 1 p. 107. [53]
[54] Maloy, Analysis: Critiquing the Empirical Evidence ; Does Involuntary Outpatient Commitment Work? Mental health Policy Resource Center (1992).
[55] Kisely S, Campbell LA, Preston N. Compulsory community and involuntary outpatient treatment for people with severe mental disorders. The Cochrane Database of Systematic Reviews 2005, Issue 3.
[56] International experiences of using community treatment orders, by the Institute of Psychiatry at the Maudsley (UK), March 2007.
