I have been specifically researching the effects of psychotropic medication on mental health outcomes, and how the use of such drugs may help or hinder positive outcomes for over a 15 years. 

1-5. blank

6. Prior to researching upon the effects of psychotropic medications in therapy, I shared conventional beliefs about the nature of severe mental illness, such as Bipolar, Schizophrenia, Schizoaffective Disorder, Major Depressive Disorder, and the need for patients so diagnosed to be on psychotropic medications, sometimes for life.  I had been formally 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 psychotic patients that raised questions about this model of care.  First, in 1994, Harvard researchers reported that outcomes for those patients with psychosis 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 (WHO) 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. I will use the term neuroleptic and atypical from hereinafter, as the term “antipsychotic” evokes an unjustified analogy of healing potential similar to antibiotics. 


II. Overview of Research Literature- Standard Antipsychotic Medications


8. Despite patients with psychosis being told they 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 with psychosis had, in fact, overactive dopamine systems[4]. In fact, attempts to quantify D2 receptor density in vivo with PET scans have also proved inconclusive results.[5] 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…retains little credibility for psychiatrists.[6]  With regards to Serotonin, Dr. Steven Rose, a Professor and neuroscientist at Open University, UK, reported a study of serotonin levels in psychiatric patients compared with psychiatric nursing staff. Both groups had the same levels, but only the patients reported feeling depressed. [7]


Dr. William Wirshing, professor at UCLA and a leading psychiatric researcher, publically announced in 1999: “We have been lying to the public about the chemical imbalance theory of mental illness”[8], and in 2011  Dr. Ronald Pies, editor-in-chief emeritus of the Psychiatric Times indicated: “In truth, the ‘chemical imbalance’ notion was always a kind of urban legend- never a theory seriously propounded by well-informed psychiatrists.”[9]


9. Since people struggling with psychosis have no known “chemical imbalance” in the brain, neuroleptic and atypical 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, standard antipsychotics (also known as older 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.[10] This thwarting of normal dopamine transmission is what causes the drugs to be so problematic in terms of their side effects.


The effects can often be seen at certain levels of blockage, and apply equally to typical and atypical neuroleptics:

prolactin elevations begin at 72% blockade[11]
extrapyramidal motor disturbances and akathisia > 78% [12]
clinically significant dysphoric reactions (listless, dejected) > 70% [13]
cognitive impairments > 70% [14]
aggravation of depressive and “negative” symptoms, so-called neuroleptic induced negative symptoms, also known as neuroleptic-induced-deficit syndrome > 70% (NIDS)[15] [16]



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 the drugs are more effective than placebo in curbing psychotic symptoms over the short term (six weeks).[17], [18]


b) Second, researchers have found that if patients abruptly quit taking antipsychotic medications, they are at high risk of relapsing. [19], [20], [21]


11. Although the studies cited above provide a rationale for continual drug use, there is a long line of evidence in the research literature starting to become known at large; however, often still not generally known by the public or even by most psychiatrists, that shows 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 negative effects (side effects).

c) They can 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.[22]   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.[23]  This was also the first evidence of how the neurological damage that caused the positive behavioral appearance was actually in fact slowly causing a worsening of long term outcomes.  The Schooler researchers were so surprised, they stated they were “unprepared to recommend placebo as treatment of choice.”


13. In the 1970s, the NIMH then 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.[24], [25], [26]  In the 1977 Dr. William Carpender study, 49 psychotic patients were placed into an experimental hospital program that provided them with psychosocial support and were then randomized them into a drug or non-drug cohort. 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.

In the 1978 study, Dr. Maurice Rappaport and his colleagues at the University of California, San Francisco randomized 80 young psychotic males admitted to Agnews State Hospital to drug and non-drug groups. Only 27% of the drug-free patients relapsed in the three years following discharge, compared to 62% of the medicated group. Most notably, only two of 24 patients (8 percent) who weren’t medicated in the hospital and continued to forgo such treatment after discharge subsequently relapsed. At the end of the study, this group of 24 drug-free patients was functioning at a dramatically higher level than drug-treated patients.

The three findings confirming the more beneficial non-drug group, led Dr. Carpenter to conclude that antipsychotic medication may make some “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%  to 90%.[27] 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. [28]


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.[29], [30], [31]  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.[32]

            This is analogous to what happens in tardive dyskinesia (TD), in which dopaminergic (DA) receptors in the nigro neostriatal pathway are up-regulated (i.e. the DA receptors become more numerous and sensitive) secondary to chronic DA blockade, thereby causing the random purposeless movements seen in TD, the Dopaminergic receptors in the mesolimbic pathway (thought to mediate the positive symptomatology, such as voices and delusions) become more sensitized and numerous (i.e. up-regulated).

When the person removes the neuroleptic-Dopaminergic blocking agent, particularly abruptly, it 'unmasks' the now up-regulated Dopaminergic receptors resulting in a 'tardive’ or ‘rebound’ or ‘supersensitivity’ psychosis.[33] The “oppositional tolerance” is created by the continuation of the drug treatment, and is producing “...the opposite of what the medication originally produced….[and causes] a worsening of the illness, [which] continues for a period of time after discontinuation of the medication, and may not be reversible.”[34]

            Researchers have found the same is true for other categories of psychiatric medications, including antidepressant medications, such as Selective Serotonergic Reuptake Inhibitors.[35], [36]  In those cases, they call the upregulation of the serotonergic system, “Tardive dysphoria,” [37] and “oppositional tolerance.” [38], [39]  The researchers note, “in the era prior to pharmacotherapy, poor outcome in mania was considered a relatively rare occurrence, however, modern outcome studies have found that a majority of bipolar patients evidence high rates of functional impairment.” Many researchers consider manic-like behaviors on a continuum with schizophrenic-like behaviors.  Researchers discussed the deterioration in outcomes by concluding that “medication-induced changes” may be at least partly responsible for the worsening outcomes. Antidepressants may cause a “worsening of the course of illness” while the antipsychotics may lead to more “depressive episodes” and “lower functional recovery rates.” Negative drug effects (side effects) may “explain the cognitive deficits in bipolar disorder patients.” [40]  These Harvard researchers note “neuropharmacological-neurotoxic factors” might be causing “cognitive deficits” in patients.[41]



IV. Research Showing that Recovery Rates are Higher for Non-Medicated or Minimally and Short Term Medicated Patients than for Standard Maintained Medicated Patients (i.e. better functioning and competency).


16. The studies cited above show that psychotropic medications increase the chronicity of psychotic symptoms over the long term. There are also a number of studies documenting long- term recovery rates are much higher for patients who do not utilize antipsychotic medications. Specifically:


a) In 1994, Courtenay Harding at Boston University reported on the long-term outcomes of 82 chronic psychotic patients discharged from Vermont State Hospital in the late 1950s and early 1960’s. She found that one-third of this cohort had recovered completely and were asymptomatic, and that all who did shared one characteristic: They had all stopped taking antipsychotic medication.  The notion that psychotic people needed to stay on antipsychotics all their lives was a “myth,” Harding said.[42], [43], [44]


b) Despite claims that medications and hospitalization are effective for treatment, in 1998 University of Cincinnati psychiatrists found that only 24% of their bipolar patients were “functionally recovered” at the end of one year.[45] 


c) In the World Health Organization studies, which covered over 1,300 patients from 10 countries, 63.7% 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 36.9% of patients had good outcomes, and the remaining patients did not fare so well. In the undeveloped countries like India, Nigeria and Columbia, only 16% of patients were regularly maintained on antipsychotics, versus 61% of patients in the developed countries.


d) In response to this body of literature, physicians and treatment teams 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.[46], [47],  [48], [49]  In particular, Cullberg noted after one year of initial onset, “remarkable self-curing capacity” for patients with psychosis if they were given psychosocial support with optimal overnight facilities.[50]  Jaakko Seikkula then more 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 took and or were are on antipsychotic medications.[51]


e) In 2007, NIMH funded researcher Martin Harrow, University of Illinois Medical School, reported on the long-term outcomes of 145 psychotic patients in the Chicago that had been naturally tracked for 15 years (late 1980’s). All patients were treated with neuroleptic medications and Harlow followed up at regular intervals.  They found that 40% of those who refused to take their antipsychotic medications were recovered at five-year and 15-year follow-up exams, versus only five percent of the medicated patients, and that, those with “other psychotic disorders” also fared much better without the use of neuroleptic or atypical medications.[52]


f) In 2013, Dutch researcher Wunderink published the results of a “gold standard” randomized controlled study to assess if neuroleptic or atypical medication specifically could be leading to a worsening of outcomes.  Wunderink randomized 128 first episode psychotic patients following six months of neuroleptic or atypical medication usage to either a Drug Reduction taper off group (DR) or Drug Maintenance stay on group (MT).  At the end of seven years, the taper off group had much higher recovery and functional outcome rates (40% versus 17%), lower relapse rates.  When data from the patients who took themselves off the drugs (N=34), regardless of which group, were assessed to those who were regularly maintained on the antipsychotic medications (N=69), the symptomatic remission rate for all patients who stopped all medications was 85% (compared to 59%), the functional remission was 56% versus 22%, and the full recovery rate was 60% versus 17%.  Wunderick’s study indicates antipsychotics lower long-term recovery due to “antipsychotic postsynaptic blockage of the dopamine signaling system, particularly the mesocortical and mesolimbic tracts…compromising important mental functions, such as alertness, curiosity, drive, and activity levels and aspects of executive functional capacity…” [53]


g) In late 2015, chairperson of psychiatry at Hofstra North Shore-LIJ School of Medicine conducted one of the most rigorous controlled studies in the United States, a two year NIMH funded study with 404 first episodic psychotic patients from 21 states, [54] a program with similar interventions to the Australia and Scandinavia programs noted above.  The Recovery After an Initial Schizophrenia Episode-RAISE study indicated first episodic psychotic patients using the NAVIGATE program, whereby they focused upon: 1) reducing dosing of antipsychotic medications by 20-50%, 2) providing individual psychotherapy and family therapy, 3) providing psycho-education and 4) providing employment-education programming), the RAISE group had significantly less psychotic and depressive symptoms, greater improvement in quality of life (10 versus 16 on 126 point scale), less likely to be re- hospitalized for psychiatric reasons, and were significantly more likely to be working and going to school.  The effects were more pronounced for shorter duration of psychosis before intervention.  Dr. Kane, lead researcher, stated in order to minimize the “bad effects of the drugs those in the new treatment group received the lowest doses possible- up to 50% less than what is prescribed in standard treatments.” [55] 


Other researchers noted this type of intervention “may be cost effective in the long run,” [56] as treatment for Schizophrenia accounts for approximately 30 percent of the 104 billion spent on mental health in the United States.[57]  That figure did not include the billions spent due to medical complications as a result of medication side effects or legal expenses from lawsuits.


h) In April of 2017, Danish researchers published the results of a 10 year follow-up study assessing the positive outcomes of 303 newly diagnosed Danish OPUS-cohort schizophrenia spectrum patients, aged 18-45.  The OPUS-cohort was a randomized clinical trial for intensive early intervention.  Of the 121 patients off all medications, by comparison to the 182 taking antipsychotic medications; 74% of the Off-Medication group were in remission (90 of 121), while only 49% of the On-Medication patients found remission (90 of 182).  Being female, having higher functioning prior to onset, having vocational/educational/employment, and staying off psychotropic medications (having the lowest symptom scores of all catergories) where the significant factors for symptom remission.  There was no positive relationship for age of onset, high school completion and premorbid IQ; however, the longer the duration prior to some treatment, the worse the outcome.  The researchers concluded that the Off-Medication group was able to function higher, had fewer negative symptoms and was able to be employed a significantly higher rate. [58]



V. Harmful Side Effects from Antipsychotic Medications


17. In addition to making patients chronically ill, patients with psychosis today suffer from a host of physical illnesses– cardiovascular problems, obesity, thyroid dysfunction, etc.– which, researchers admit, are due to “toxicity from medications.” [59]


More 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.”[60] 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..[61] The risk of developing this possible life threatening effect from the neuroleptic or atypical medication increases with higher doses and longer duration.[62]


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 and is a cause of suicide.[63], [64], [65], [66], [67]


c) Emotional impairment. Many patients describe feeling like “zombies” on the medications. 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.[68] The quality of life on conventional neuroleptics, researchers agreed, is “very poor.” [69]


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.”[70] 


e) Other side effects of standard neuroleptics include a vast array of negative effects on a striking number of physical systems. These include drowsiness, dizziness, nausea, vomiting, diarrhea, constipation, heartburn, dry mouth, increased saliva production, increased appetite, weight gain, stomach pain, anxiety, agitation, restlessness, difficulty falling asleep or staying asleep, decreased sexual interest or ability, vision problems, muscle or joint pain, dry or discolored skin, difficulty urinating, muscle stiffness, confusion, fast or irregular pulse, sweating, unusual and uncontrollable movements of face or body, faintness, seizures, Parkinsonian symptoms such as slow movements or shuffling walk, hives, itching, difficulty breathing or swallowing, gynecomastia in male children, painful erection of penis lasting for hours.  Additionally, 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.[71], [72], [73]


f) Suicide: Schizophrenia patients now commit suicide at 20 times the rate they did prior to the use of neuroleptics, and when researcher’s completed the largest study ever done to address suicide in psychotic patients, they concluded that the 10% lifetime rate of suicide is incorrect, noting it is approximately 4%, and that psychiatric medications appears to be a causal factor for suicide. [74]  When researchers compared typical hospital treatment with neuroleptic or atypical medications against non-psychiatric psychological interventions over an 11 month period, pure psychological interventions were less likely to produce suicides (3 suicides compared to none in the pure psycho-social treatment group).[75], [76] 


g) Death: During a 17 year follow up study that involved 99 people diagnosed with psychosis, 39 of the patients died; however, when researchers accounted for age, gender, somatic diseases, blood pressure, cholesterol, body mass index, smoking, exercise, alcohol, education and other premature death factors, the relative risk was 2.50 times greater (95% confidence level) if the patient took just one neuroleptic at baseline.[77] 


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, Prolixin 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.”[78]


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.[79], [80], [81], [82], [83] 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.”[84] 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.”


Researchers now have learned that Risperdal was no better than older drugs and that the “unethical marketing” and “poor scientific bases” used to create treatment guidelines lead to the massive distribution, harm and lawsuits regarding neuroleptic or atypical medications.[85] 


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.[86]


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.”[87]


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.[88]


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.[89] 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 more growing evidence that the neuroleptic or 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.


Researcher Waddington in 1998 followed 88 patients over a 10 year period and noted that 39 of them died, however, he discovered that of those who died, it was caused by taking two or more neuroleptic or atypicals over the time and the patient was later so burdened with chronic physical illnesses, it replaced the “psychiatric disorder as the primary focus of medical care.” He concluded that the final pathway to death for the psychiatric treated patient was “global medical decline” and or respiratory illness following medication usage.[90]


A few years later in 1991, researchers surveyed 49 cases of sudden death and indicated that in 46 of the 49 cases of sudden death reported, the psychiatric medications were indicative of the cause. [91] 


In a 2003 Irish study, 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. [92]  


In 2014, Gerhard et al, studied over 136,000 above 65 year old first contact with antipsychotic medication patients in an attempt to estimate the comparative mortality risk between differing antipsychotic medications.  Over the six month assessment period, they found a positive causal dose-response increase mortality effect (i.e. the higher the dosing, the more likely a patient would die within the six months) and noted that significant variation in mortality affects survival rates for those patients taking these medications.[93]  They also noted prior meta-analysis research of 15 clinical trials, and found a 50% increase in mortality for patients taking newer antipsychotic medications[94], but that subsequent observational studies found similar mortality risks for first generation antipsychotic medications,[95] [96] [97] whereby the United Kingdom and United States started issuing warnings about the increased mortality for using antipsychotic medications.


Finally, in 2016, Parkinson disease researchers at the VA Center for Clinical Management Research  noted that of the 7,900 VA patients that took typical and atypical antipsychotic medications (Thorazine, Haldol, Risperdal, Zyprexa, Seroquel), they were twice as likely to die over six months as those who did not take antipsychotic medications, and the researchers noted prior research reviewing 17 placebo-controlled studies found similar results that antipsychotics carried approximately twice the likelihood of mortality in demented elderly.[98] Although the authors note the their 2016 study data is correlational, they did note that antipsychotics can worsen Parkinson's disease and that as many as 60% of patients can development psychosis and 80% can develop dementia at some point prior to death, which coincides with prior noted researcher’s indicating using antipsychotic medications can cause patients to develop prolonged psychosis.


[1] Hegarty, J, et al. (1994) “One hundred years of schizophrenia: a meta-analysis of the outcome literature.” American Journal of Psychiatry, 151:1409-16.

[2] Leff, J., et al. (1992) “The international pilot study of schizophrenia: five-year follow-up findings.” Psychological Medicine, 22:131-45.

[3] Jablensky, A., et al. (1992) “Schizophrenia: manifestations, incidence and course in different cultures, a World Health Organization ten-country study.” Psychological Medicine, monograph supplement:. 20:1-95.

[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] 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.

[6] Deniker, P. (1990).“The neuroleptics: a historical survey.” Acta Psychiatrica Scandinavica, supplement 358. 82:83-87.

[7] Rose, N. (2005). Biological Citizenship, in Aihwa Ong and Stephen Collier, eds., Global Assemblages: Technology, Politics and Ethics as Anthropological Problems, pp. 439-463. Oxford: Blackwell.

[8] Wirshing, W., Personal Communication at Lecture at UCLA in 1999.

[9] Pies, R.,  Psychiatry’s new brain-mind and the legend of the chemical imbalance, In Psychiatric Times, July 11, 2011.  Online

[10] Wysong, P., (2000). PET Brain Scans Best to Determine Schizophrenics’ drug dosages, In Washington Post, April 12, 2000, Vol. 36, Issue 14.

[11] Kapur S, Zipursky R, Jones C, Remington G, Houle S. (2000) Relationship between dopamine D(2) occupancy, clinical response, and side effects: a double-blind PET study of first-episode schizophrenia. Am J Psychiatry 2000;4:514–20

[12] Kapur S, Zipursky R, Jones C, Remington G, Houle S. (2000) Relationship between dopamine D(2) occupancy, clinical response, and side effects: a double-blind PET study of first-episode schizophrenia. Am J Psychiatry 2000;4:514–20

[13] Mizrahi R, Rusjan P, Agid O, Graff A, Mamo DC, Zipursky RB, Kapur S. (2007) Adverse subjective experience with antipsychotics and its relationship to striatal and extrastriatal D2 receptors: a PET study in schizophrenia. Am J Psychiatry 164(4):630-7

[14] Mizrahi R, Rusjan P, Agid O, Graff A, Mamo DC, Zipursky RB, Kapur S. (2007) Adverse subjective experience with antipsychotics and its relationship to striatal and extrastriatal D2 receptors: a PET study in schizophrenia. Am J Psychiatry 164(4):630-7

[15] de Haan L, van Bruggen M, Lavalaye J, Booij J, Dingemans PM, Linszen D (2003) Subjective experience and D2 receptor occupancy in patients with recent-onset schizophrenia treated with low-dose olanzapine or haloperidol: a randomized, double-blind study. Am J Psychiatry 160:303– 309

[16] Voruganti L, Slomka P, Zabel P, Costa G, So A, (2001) Mattar A, Awad AG: Subjective effects of AMPT-induced dopamine depletion in schizophrenia: correlation between dysphoric responses and striatal D(2) binding ratios on SPECT imaging. Neuropsychopharmacology 25:642–650

[17] Cole, J, et al. (1964). “Phenothiazine treatment in acute schizophrenia.” Archives of General Psychiatry, 10:246-61.

[18] Adams, (2005). “Chlorpromazine for Schizophrenia: A Cochrane systematic review of 50 years of randomized controlled trials.” BMC Medicine, 3:15.

[19] Gilbert, P, et al. (1995).“Neuroleptic withdrawal in schizophrenic patients.” Archives of General Psychiatry, 52:173-188.

[20] Prien, R. (1968).“Relapse in Chronic Schizophrenics following Abrupt Withdrawal of Tranquilizer Medication.”  British Journal of Psychiatry, 115, 679-86).

[21] Baldessarini, R. J. (1995). Neuroleptic withdrawal in schizophrenic patients.  Archives of General Psychiatry, 52:189-191.


[22] Cole, J, et al. (1964). “Phenothiazine treatment in acute schizophrenia.” Archives of General Psychiatry, 10:246-61.

[23] Schooler, N, et al. (1967). One year after discharge: community adjustment of schizophrenic patients. American Journal of Psychiatry, 123:986-95 (quote: pg 991).

[24] Rappaport, M, et al. (1978). “Are there schizophrenics for whom drugs may be unnecessary or contraindicated?” International Pharmacopsychiatry ,13:100-11.

[25] Carpenter, W, et al. (1977). “The treatment of acute schizophrenia without drugs.” American Journal of Psychiatry, 134:14-20.

[26] Bola J, et al. (2003). “Treatment of acute psychosis without neuroleptics: two-year outcomes from the Soteria project.” Journal of Nervous Mental Disease, 191:219-29.

[27] Silvestri S, Seeman MV, Negrete JC et al. (2000). "Increased dopamine D2 receptor binding after long-term treatment with antipsychotics in humans: a clinical PET study". Psychopharmacology, 152: 174–80. doi:10.1007/s002130000532. PMID 11057521.

[28] Chouinard, G, et al. (1978). “Neuroleptic-induced supersensitivity psychosis.” American Journal of Psychiatry, 135:1409-10. Also see Chouinard, G, et al. (1980).“Neuroleptic-induced supersensitivity psychosis: clinical and pharmacologic characteristics.”  American Journal of Psychiatry, 137:16-20.

[29] Gur, R, et al. (1998). “A follow-up magnetic resonance imaging study of schizophrenia.” Archives of General Psychiatry, 55:142-152.

[30] Chakos M, et al. (1994).“Increase in caudate nuclei volumes of first-episode schizophrenic patients taking antipsychotic drugs.” American Journal of Psychiatry, 151:1430-6.

[31] Madsen A, et al. (1998). “Neuroleptics in progressive structural brain abnormalities in psychiatric illness.” The Lancet, 352:784-5.

[32] Gur, R, et al. (1998).  “Subcortical MRI volumes in neuroleptic-naive and treated patients with schizophrenia.” American Journal of Psychiatry, 155:1711-17.

[33] Samaha, A., Seeman, P., et al. (2007). “Breakthrough Dopamine Supersensitivity during Ongoing Antipsychotic Treatment Leads to Treatment Failure over Time.”  Journal of Neuroscience, 27: 2979-2986.

[34] El-Mallakh, R. “Tardive dysphoria: The role of long-term antidepressant use in inducing chronic

   depression. Medical Hypotheses 76 (2011): 769-773.

[35] E. Richelson, (1991). “Biological basis of depression and therapeutic relevance,” Journal of Clinical Psychiatry,  52(6):4–10.

[36] Cooper, J., Bloom, F.,, and Roth, R.. (1996). The Biochemical Basis of Neuropharmacology, Oxford University Press, New York, NY, USA.

[37] El-Mallakh, R.S., Gao, Y. and Roberts, J. (2011)., Tardive dysphoria: The role of long term antidepressant use in-inducing chronic depression.  Medical Hypotheses, 76(6):769–773.

[38] Andrews, P.W., Kornstein, S.W.,Halberstadt, L. J., et. al. (2011). Blue again: perturbational effects of antidepressants suggest monoaminergic homeostasis in major depression. Frontiers in Psychology, 159(2): 1-24.

[39] Fava, G.A., & Offidani, E. (2011)). The mechanisms of tolerance in antidepressant action, Progress in Neuro-Psychopharmacology and Biological Psychiatry. 35:1593–1602.

[40] Zarate, C. (2000). Functional impairment and cognition in bipolar disorder  Psychiatric Quarterly 71:309-29.

[41] Huxley, N. (2007). Disability and its treatment in bipolar disorders. Bipolar Disorders. 9:183-96.

[42] Harding, C. (1987). The Vermont longitudinal study of persons with severe mental illness. American Journal of Psychiatry, 144:727-34.

[43] Harding, C. (1994). Empirical correction of seven myths about schizophrenia with implications for treatment. Acta Psychiatrica Scandinavica, 90(384):140-6.

[44] McGuire, P. (2000). New hope for people with schizophrenia,” APA Monitor, 31.

[45] Keck, P. (1998). 12-month outcome of patients with bipolar disorder following hospitalization for a manic or mixed episode. American Journal of Psychiatry, 155:646-52.

[46] Ciompi, L, et al. (1992).  The pilot project Soteria Berne.  British Journal of Psychiatry 161, supplement 18:145-53.

[47] Cullberg J. (1999). Integrating psychosocial therapy and low dose medical treatment in a total material of first-episode psychotic patients compared to treatment as usual. Medical Archives 53:167-70.

[48] Cullberg J. (2002). One-year outcome in first episode psychosis patients in the Swedish Parachute Project.  Acta Psychiatrica Scandinavica, 106 :276-85.

[49] Lehtinen V, et al. (2000). Two-year outcome in first-episode psychosis according to an integrated model. European Psychiatry, 15:312-320.

[50] Cullberg, J., Levander S. Holmqvist. R, et al. One-year outcome in first-episode psychosis patients

    in the Swedish Parachute Project. Acta Psychiatr Scand. 2002; 106: 276-285.

[51] Seikkula J, et al. (2006). Five-year experience of first-episode nonaffective psychosis in open-dialogue approach. Psychotherapy Research, 16(2): 214-228.

[52] Harrow M, et al.  (2007). Factors involved in outcome and recovery in schizophrenia patients not on antipsychotic medications. Journal of Nervous and Mental Disease, 195: 406-414.

[53] Wunderink, L, Nieboer, R. et al, “Recovery in Remitted First Episode Psychosis at 7 Years of Follow-up of an Early Dose Reduction/Discontinuation of an Early Dose Reduction/Discontinuation of Maintenance Treatment Strategy: Long-term Follow-up of a 2 Year Randomized Clinical Trial”, JAMA Psychiatry. 2013, Online July 3, 2013.

[54] Kane, J., Robinson, D., et al, “Comprehensive Versus Usual Community Care for First Episode Psychosis: 2-Year Outcomes From the NIMH RAISE Early Treatment Program”, Am J Psych, 2015, Online October 24, 2015.

[55] Karter, J. “Confusion over antipsychotic dosing data in RAISE study”, Mad In America, In the News, October 21, 2015.  Online October 24, 2015.

[56] Bernstein, L., Study suggests new way to treat people after first schizophrenia episode”, The Washington Post, October 24, 2015. Online.

[57] Mark T, Coffey R, et al. “U.S. Spending For Mental Health and Substance Abuse Treatment, 1991-2001”.  2005 Jan-Jun Suppl Web Exclusives, W5-133-W135-142.

[58] Wils, R. S., Gotfredsen, D. R., Hjorthøj, C., Austin, S. F., Albert, N., Secher, R. G., … & Nordentoft, M. (2016). Antipsychotic medication and remission of psychotic symptoms 10years after a first-episode psychosis. Schizophrenia Research.(Abstract)

[59] Kupfer, D. (2005). The increasing medical burden in bipolar disorder. JAMA,  293(20): 2528-2530.

[60] Crane, G. (1973). Clinical psychopharmacology in its 20th year. Science, 181:124-128. Also see American Psychiatric Association, Tardive Dyskinesia: A Task Force Report (1992).

[61] Correll CU, Leucht S, Kane JM. Lower risk for tardive dyskinesia associated with second-generation antipsychotics: a systematic review of 1-year studies. Am J Psychiatry. 2004;161(3):414-425

[62] Crimson ML, Argo TR, Buckley PF. Schizophrenia. In: DiPiro JT, Talbert RL, Yee GC, et al, eds. Pharmacotherapy: a pathophysiologic approach. 8th ed. New York, NY: McGraw- Hill; 2011:1147-1172.

[63] Shear, K et al. (1982). Suicide associated with akathisia and deport fluphenazine treatment. Journal of Clinical Psychopharmacology, 3:235-6.

[64] Van Putten, T. (1987). Behavioral toxicity of antipsychotic drugs. Journal of Clinical Psychiatry, 48:13-19.

[65] Van Putten, T. (1975). The many faces of akathisia. Comprehensive Psychiatry ,16:43-46.

[66] Herrera, J. (1998). High-potency neuroleptics and violence in schizophrenia. Journal of Nervous and Mental Disease, 176:558-561.

[67] Galynker, I. (1997). Akathisia as violence. Journal of Clinical Psychiatry, 58:16-24.

[68] Van Putten, T. (1979). The board and care home. Hospital and Community Psychiatry, 30:461-464.

[69] Weiden P. (1996). Atypical antipsychotic drugs and long-term outcome in schizophrenia. Journal of Clinical Psychiatry, 57(11):53-60.

[70] Keefe, R. (1999). Do novel antipsychotics improve cognition? Psychiatric Annals, 29:623-629.

[71] Arana, G. (2000). An overview of side effects caused by typical antipsychotics. Journal of Clinical Psychiatry 61(8):5-13.

[72] Waddington, J. (1998). Mortality in schizophrenia. British Journal of Psychiatry,173:325-329.

[73] Joukamaa, M, et al. (2006) Schizophrenia, neuroleptic medication and mortality. British Journal of Psychiatry, 188:122-127.

[74] Healy, D et al. (2006). Lifetime suicide rates in treated schizophrenia. British Journal of Psychiatry, 188:223-228.

[75] Healy, D et al. (2006). Lifetime suicide rates in treated schizophrenia. British Journal of Psychiatry, 188:223-228.

[76] Deikman, A., Whitaker, L. (1979).  Humanizing the Psychotherapy Ward: Changing from Drugs to Psychotherapy. Psychotherapy: Theory, Research, and Practice, 16 (2): 204-214.

[77] Joukamaa, M., Heliovaara, M., et al. (2006). Schizophrenia, neuroleptic medication and mortality. British Journal of Psychiatry, 188:122-127.

[78] FDA approval letter from Robert Temple to Janssen Research Foundation, December 21, 1993.

[79] Rosebush, P. (1999). Neurologic side effects in neuroleptic-naïve patients treated with haloperidol or risperidone. Neurology, 52:782-785.

[80] Knable, M.  (1997). Extrapyramidal side effects with risperidone and haloperidol at comparable D2 receptor levels. Psychiatry Research: Neuroimaging Section, 75:91-101.

[81] Sweeney, J. (1997). Adverse effects of risperidone on eye movement activity. Neuropsychopharmacology, 16:217-228.

[82] Carter, C. (1995) Risperidone use in a teaching hospital during its first year after market approval. Psychopharmacology Bulletin, 31:719-725.

[83] Binder, R. (1998). A naturalistic study of clinical use of risperidone. Psychiatric Services, 49 :524-6.

[84] Mattes, J. (1997). Risperidone: How good is the evidence for efficacy? Schizophrenia Bulletin, 23:155-161.

[85] Caplan, P., “Diagnosisgate: Conflict of Interest at the Top of Psychiatric Apparatus.”  APORIA, Jan. (2015); 30-41.

[86] Whitaker, R. (2002). Mad in America. New York: Perseus Press. pp:279-281.

[87] Geddes, J. (2000). Atypical antipsychotics in the treatment of schizophrenia.  British Medical Journal, 321:1371-76.

[88] Lieberman, J, et al. (2005). Effectiveness of antipsychotic drugs in patients with schizophrenia. New England Journal of Medicine 353:1209-1233.

[89] Davies, L, et al. (2007). Cost-effectiveness of first- v. second-generation antipsychotic drugs. The British Journal of Psychiatry, 191:14-22.

[90] J. Waddington, "Mortality in Schizophrenia," British Journal of Psychiatry, 173 (1998), 325-329. 

[91] Mehtonen OP; Aranko K; M¨alkonen L; Vapaatalo H. Acta Psychiatr Scand, 84(1):58-64 1991 Jul.

[92] Morgan, M, et al. “Prospective analysis of premature morbidity in schizophrenia in relation to health service engagement." Psychiatry Research 117 (2003):127-35.

[93] Gerhard T, et al. Comparative mortality risks of antipsychotic medications in community-dwelling older adults.  BJP, Jul 2014, 205 (1) 44-51; DOI: 10.1192/bjp.bp.112.122499.

[94] Schneider LS, et al. Risk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomized placebo-controlled trials. JAMA 2005; 294: 1934-43.

[95] Wang PS, Schneeweiss S,, et al. Risk of death in elderly users of conventional vs. atypical antipsychotic medications. N Engl J Med 2005; 353: 2335–41.

[96] Gill SS, Bronskill SE, , et al. Antipsychotic drug use and mortality in older adults with dementia. Ann Intern Med 2007; 146: 775–86.

[97] Kales HC, Valenstein M, et al. Mortality risk in patients with dementia treated with antipsychotics versus other psychiatric medications. Am J Psychiatry 2007; 164: 1568–76.

[98] Baron, M. et al. “Antipsychotics and increased mortality: Are we sure?” JAMA Neurology, online March 21, 2016,

 [TW1]Was statistically significant, but 10 versus 16 (NAVIGATE) on a 126 pt scale seems clinically non significant. 

Psychological – Social- Cultural Factors in the Development of Schizophrenia

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).

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

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

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

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

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)

"...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"

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).

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.

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.

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:
"Cognitive Therapy for Psychosis: A Formulation-Based Approach" by Anthony
Morrison, Julia Renton, Hazel Dunn, Steve Williams & Richard Bentall,
published in 2004 by Brunner-Routledge.

Social causation versus social selection
There has been an ongoing debate between those who view social factors as
influencing the development of schizophrenia (social causation) and those
who understand individuals at risk to choose adverse social environments
(social selection). A number of the research findings just described
cannot be accounted for by social selection theorists. Boydell et al
(2001) found that non-white minorities to be at higher risk when they were
in a smaller minority even though they lived in an area of higher social

Boydell et al (2004) concluded:
"It is now clear, however, that, in order to understand the causes of
schizophrenia, the role of the social environment cannot be continued to
be ignored. In saying this, we are not proposing an oppositional social
instead of biological approach, which we consider as futile as arguing
whether poverty or mycobacteria cause tuberculosis! Rather, we suggest
that both social and biological factors need to be studied as well as
their interaction.

We need to recognize that (i) social factors can impact on brain
development, (ii) some social factors give rise to psychological
vulnerabilities, and (iii) many social factors act over the life course,
creating developmental liabilities...It is possible that the social
environment creates psychological vulnerabilities that act additively to
the risk function in combination with genetic or non-genetic
neurodevelopmental impairments...

The challenge for schizophrenia researchers in the coming decade is first
distinguish those candidate social factors that do contribute to
schizophrenia risk from those that do not and, second, to identify the
interplay between these factors, genetic susceptibility, and their
respective effects on, and interactions with, brain development" (PP.


Irwin, M. (2004).  Reversal of schizophrenia without neuroleptics.  Ethical Human Psychology and Psychiatry, 6(1).
Irvin, M., (2004) “Treatment of Schizophrenia Without Neuroleptics: Psychosocial Interventions Versus Neuroleptic Treatment”,

Randomized studies comparing psychosocial treatment programs without neuroleptics to drug-based programs were sought out for review, and six were found.  Long-term outcomes were statistically equivalent or superior in the non-drug group in all six studies, even those where the quality of the psychosocial treatment was questionable.  In studies with psychosocial interventions that appeared to have higher quality, both short and long-term results were equivalent or superior without neuroleptics.  These findings suggest that neuroleptics interfere with long-term recovery and, if appropriate psychosocial interventions are available, are not even necessary for short-term behavior control.

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 these had statistically superior outcomes in the non-drug 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.

Seikkula, et al, (2003) Open Dialog Approach: Treatment Principles and Preliminary Results of a 2 Year Follow UP on First Episode Schizophrenia, in Ethical and Human Sciences and Services, 5 (3), 163-182.
I think the most recent results were 82% did not have psychotic symptoms at the end of five years, 86% had returned to their studies or jobs, and  only 14% were on disability allowance. Only 29%  had ever been exposed to a neuroleptic medication  at all during the five years, and only 17% were  on neuroleptics at the end of five years.


Seikkula J, Alakare B & Aaltonen J (2000) A two year follow-up on open dialogue treatment in first episode psychosis: need for hospitalization and neuroleptic medication decreases. Social & Clinical Psychiatry 10 (2) 20-29.
Open dialogue, a rapid response service based on psychological principles, has led to much shorter
inpatient treatments, a significant reduction in the use of psychotropic medication, an increase in employment of those who have suffered psychological distress, a return to education of young people with psychological problems, and a significant fall in the incidence of schizophrenia.

G. Haddock, S. Lewis, R. Bentall, G. Dunn,R. Drake and N. Tarrier, Royal College of Psychiatrists Influence of age on outcome of psychological treatments in first-episode psychosis, In The British Journal of Psychiatry (2006) 188: 250-254. doi: 10.1192/bjp.188.3.250 ]

Psychological treatments have been shown to be effective  in patients with psychosis.  Randomized controlled, evaluate the effectiveness of cognitive-behavioral therapy (CBT), supportive counseling and treatment as usual.
Younger responded better to supportive counseling than CBT over 3 months.

Older participants responded better to CBT than to supportive counseling over 18 months.
Younger participants showed a greater increase in insight after CBT compared with treatment as usual and supportive counseling, and were more difficult to engage in therapy.

Young people may have different needs with regard to engagement in psychological treatments. Treatment providers need to take age-specific factors into account.


Family Counseling/Therapy & Education

J Leff, L Kuipers, R Berkowitz and D Sturgeon         The British Journal of Psychiatry 146: 594-600 (1985). A controlled trial of social intervention in the families of schizophrenic patients: two year follow-up.

The two-year follow-up results are reported of a trial of social intervention in families of schizophrenic patients in high social contact with high-expressed emotion (EE) relatives. For those patients who remained on antipsychotic medication throughout the two years, the social intervention significantly reduced the relapse rate. In those experimental families where relatives' EE and/or face-to-face contact was lowered, the relapse rate was 14% compared with 78% for control patients on regular medication (P = 0.02).   no non med group.

N Tarrier, C Barrowclough, C Vaughn, JS Bamrah, K Porceddu, S Watts and H Freeman
Department of Psychology, Prestwich Hospital, Manchester. The British Journal of Psychiatry 154: 625-628 (1989).  Community management of schizophrenia. A two-year follow-up of a behavioral intervention with families.

The relapse and readmission rates of schizophrenic patients who participated in a controlled trial of a nine-month behavioral family intervention trial based on the EE status of their relatives are presented at two years. The patients who received the behavioral family intervention had lower rates of relapse and readmission than patients from high-EE homes who had received a short educational program or routine treatment. The relapse rate of the behavioral family intervention group (33%) was the same as that of the low-EE group (33%), and significantly lower than that of the non-intervention high-EE group (59%).

W Xiong, MR Phillips, X Hu, R Wang, Q Dai, J Kleinman and A Kleinman
Department of Community Medicine, Shashi City Veterans Psychiatric Hospital, China.   Family-based intervention for schizophrenic patients in China. A randomized controlled trial The British Journal of Psychiatry 165: 239-247 (1994).

BACKGROUND. We developed and evaluated a comprehensive, ongoing intervention for families of schizophrenic patients appropriate for China's complex family relationships and unique social environment. METHOD. Sixty-three DSM-III-R schizophrenic patients living with family members were enrolled when admitted to hospital and randomly assigned to receive standard care or a family-based intervention that included monthly 45-minute counseling sessions focused on the management of social and occupational problems, medication management, family education, family group meetings, and crisis intervention. RESULTS. At 6, 12, and 18-month follow-ups by blind evaluators, the proportion of subjects re-hospitalized was lower, the duration of re-hospitalization was shorter, and the duration of employment was longer in the experimental group than in the control group; these differences were statistically significant at the 12 and 18-month follow-ups and were not explained by differences in drug compliance.

J Leff, R Berkowitz, N Shavit, A Strachan, I Glass and C Vaughn
MRC Social and Community Psychiatry Unit, Institute of Psychiatry, London. The British Journal of Psychiatry 157: 571-577 (1990).  A trial of family therapy versus a relatives' group for schizophrenia. Two-year follow-up.

The results are reported of a two-year follow-up of a trial of family sessions in the home (including patients) (12 families) versus a relatives' group (excluding patients) (11 families). Subjects were patients with schizophrenia living in high face-to-face contact with high-EE relatives. Patients were maintained on neuroleptic drugs for two years where possible. Relatives' critical comments and hostility were significantly lowered by nine months, but no significant changes occurred subsequently. Relatives' over involvement reduced steadily throughout the trial, and reduction in relatives' EE, either alone or in combination with reduced face-to-face contact, appeared to be associated with a lower relapse rate. The relapse rates for patients in the family-therapy and relatives'-group streams were 33% and 36% at two years. When these data were combined with the results of a previous trial, it was found that patients in families assigned to any form of social intervention had a two-year relapse rate of 40%, significantly lower than the 75% relapse rate for patients whose families were offered no help. We therefore recommend that relatives' groups are established in conjunction with some family sessions in the home for patients at high risk of relapse.  No non medication group.

Zhang M, Wang M, Li J, et al. Randomized-control trial of family intervention for 78 first-episode male schizophrenic patients: an 18-month study in Suzhou Jiangsu. Br J Psychiatry. 1994;165:96-102.


W. R. McFarlane, E. Lukens, B. Link, R. Dushay, S. A. Deakins, M. Newmark, E. J. Dunne, B. Horen and J. Toran.  Department of Epidemiology of Mental Disorders, College of Physicians and Surgeons, Columbia University, USA.   Multiple-family groups and psycho-education in the treatment of schizophrenia.

OBJECTIVE: To compare outcomes in psychoeducational multiple-family group treatment vs psychoeducational single-family treatment. METHOD: A total of 172 acutely psychotic patients, aged 18 to 45 years, with DSM-III-R schizophrenic disorders were randomly assigned to single or multiple-family psychoeducational treatment at six public hospitals in the state of New York. Psychotic relapse, symptom status, medication compliance, rehospitalization, and employment were assessed independently during 2 years of supervised treatment. RESULTS: The multiple-family groups yielded significantly lower 2-year cumulative relapse rates than did the single-family modality (16% vs 27%) and achieved markedly lower rates in patients whose conditions had not remitted at index hospital discharge (13% vs 33%). The relapse hazard ratio between treatments was 1:3. The relapse rate for both modalities was less than half the expected rate (65% to 80% for 2 years) for patients receiving individual treatment and medication. Rehospitalization rates and psychotic symptoms decreased significantly, and medication compliance was high, to an equal degree in both modalities. CONCLUSION: Psychoeducational multiple-family groups were more effective than single-family treatment in extending remission, especially in patients at higher risk for relapse, with a cost-benefit ratio of up to 1:34.  No non medication group.


I. R. Falloon, J. L. Boyd, C. W. McGill, M. Williamson, J. Razani, H. B. Moss, A. M. Gilderman and G. M. Simpson Family management in the prevention of morbidity of schizophrenia. Clinical outcome of a two-year longitudinal study.

Environmental stress may contribute to the clinical morbidity of established cases of schizophrenia treated with optimal neuroleptic drugs. A family-based approach that aimed to enhance the problem-solving capacity of the index patient and his family caregivers was compared with a patient-oriented approach of similar intensity over a two-year period. Thirty-six patients who returned to stressful parental households after florid episodes of schizophrenia (CATEGO and DSM-III) were stabilized with optimal neuroleptics before being randomly assigned to family or individual therapy in a comprehensive community management program. After nine months, family-managed patients had fewer exacerbations of schizophrenia, lower ratings of schizophrenic psychopathology, fewer hospital admissions, and a trend toward lower deficit symptoms and reduced neuroleptic dosage (unknown if medication reduction caused the reduction in symptoms or reduction in symptoms caused the medication reduction). This reduced clinical morbidity was sustained throughout the second year of less intensive follow-up. The relative efficacy of the family approach in this clinical management study did not appear to be due to prognostic factors, rater bias, stressful life events, or the effectiveness of pharmacotherapy. Definitive tests of these findings with respect to efficacy require further well-designed studies.


G. E. Hogarty, C. M. Anderson, D. J. Reiss, S. J. Kornblith, D. P. Greenwald, R. F. Ulrich and M. Carter
Western Psychiatric Institute and Clinic, University of Pittsburgh, School of Medicine, PA 15213.   Family psychoeducation, social skills training, and maintenance chemotherapy in the aftercare treatment of schizophrenia. II. Two-year effects of a controlled study on relapse and adjustment. Environmental-Personal Indicators in the Course of Schizophrenia (EPICS) Research Group.

We demonstrated earlier that a novel family psychoeducational approach and an individual social skills training approach designed for patients living in high-expressed emotion households each reduced schizophrenic relapse by one-half when compared with medication controls in the 1st year after hospital discharge. The combination of treatments resulted in no relapse. Results have now been obtained after 2 years of continuous treatment. By 24 months, a persistent and significant effect of family intervention on forestalling relapse was observed, but the effect of social skills training was lost late in the 2nd year. There was no additive effect on relapse that accrued to the combination of treatments. Beyond 2 years, however, the effect of family intervention was likely compromised as well. Treatment effects on the adjustment of survivors were circumscribed, due, in part, to study design characteristics. Effects generally favored the social skills-alone condition at 1 year and the family condition or combined family/social skills condition at 2 years.

Psychodynamic Approaches (each listed presents research showing approach to be effective)

Alanen, Y. O. (1997). Schizophrenia: Its Origins and Need-Adapted Treatment. London: Karnac Books.
Benedetti, G. (1987). Psychotherapy of Schizophrenia. New York: New York University Press.
Reported in Italy and Switzerland, a series of 50 severe schizophrenic cases treated with intensive psychoanalytic therapy (2-5 sessions per week) for 3 to 10 years by their supervisees, with “very good” results in 80% of the cases.

Karon, B.P., & Vandenbos, G.R. (1981). Psychotherapy of Schizophrenia: The Treatment of Choice. Northvale, NJ: Jason Aronson, Inc.

Martindale, B. et al (Eds.) (2000). Psychosis: Psychological Approaches and their Effectiveness-Putting Psychotherapies at the Centre of Treatment. UK: Gaskell for ISPS.

CBT & Psychosis (some have research data in them Daniel Freeman & Philippa Garety (2004). Paranoia: The Psychology of Persecutory Delusions. NY: Psychology Press.

Richard Bentall (2003). Madness Explained: Psychosis and Human Nature. NY: Penquin Books.

Paul Chadwick, Max Birchwood & Peter Trower (1996). Cognitive Therapy for Delusions, Voices and Paranoia. NY: John Wiley & Sons.

David Fowler, Phillipa Garety & Elizabeth Kuipers (1995). Cognitive Behaviour Threrapy for Psychosis: Theory and Practice. NY: John Wiley & Sons.

Daniel Freeman & Philippa Garety (2004). Paranoia: The Psychology of Persecutory Delusions. NY: Psychology Press.

Paul French & Anthony Morrison (2004). Early Detection and Cognitive Therapy for People at High Risk of Developing Psychosis: A Treatment Approach. John Wiley & Sons, Ltd.

John Gleeson & Patrick McGorry (Eds) (2004). Psychological Interventions in Early Psychosis: A Treatment Handbook. UK: John Wiley & Sons, Ltd

Andrew Gumley & Matthias Schwannauer (2006). Staying Well After Psychosis:
A Cognitive Interpersonal Approach to Recovery and Relapse Prevention. John Wiley & Sons, Ltd.

Gillian Haddock & Peter Slade (Eds.) (1996). Cognitive-Behavioral Interventions with Psychotic Disorders.NY: Routledge.

Chris Harrop & Peter Trower (2003). Why does Schizophrenia Develop at Late adolescence?: A Cognitive-Developmental Approach to Psychosis.UK: Wiley.

David Kingdom & Douglas Turkington (1994). Cognitive-Behavioral Therapy of Schizophrenia. NY: The Guilford Press.

David Kingdom & Douglas Turkington (2005). Cognitive Therapy of Schizophrenia. NY: The Guilford Press.

Anthony Morrison (Ed.) (2002). A Casebook of Cognitive Therapy for Psychosis. NY: Brunner-Routledge.

Carlo Perris (1989). Cognitive Therapy with Schizophrenic Patients. NY: The Guilford Press.

Carlo Perris & Patrick McGorry (Eds.) (1998).Cognitive Psychotherapy of Psychotic and Personality Disorders: Handbook of Theory and Practice. NY:
John Wiley & Sons.

Mark Reinecke & David Clark (Eds.) (2004). Cognitive Therapy Across the Lifespan: Evidence and Practice. NY: Cambridge University Press.

Additional CBT and Dynamic Treatment Approaches.

Alford, B. A. & Beck, A. T. (1997). The Integrative Power of Cognitive Therapy. NY: The Guilford Press. (This volume is not specifically concerned with psychosis, but does have a chapter on schizophrenia and other psychoses).

*Bentall, R. P. (2003). Madness Explained: Psychosis and Human Nature.London: Penguin Books.

*Chadwick,, P., Birchwood, M. & Trower, P. (1996). Cognitive Therapy for Delusions, Voices and Paranoia. NY: John Wiley & Sons.

*Fowler, D, Garety, P. A. & Kuipers, E. (1995). Cognitive Behaviour Threrapy for Psychosis: Theory and Practice. NY: John Wiley & Sons.

*Freeman, D. & Garety, P. A. (2004). Paranoia: The Psychology of Persecutory Delusions. NY: Psychology Press.

*French, P. & Morrison, A. (2004). Early Detection and Cognitive Therapy for People at High Risk of Developing Psychosis: A Treatment Appraoch. West Sussex, UK: John Wiley & Sons Ltd.

Garety, P. A. & Hemsley, D. R. (1997). Delusions: Investigations into the Psychology of Delusional Resoning. East Sussex, UK: Psychology Press.

*Gleeson, J. & McGorry, P. (Eds) (2004).  Psychological Interventions in Early Psychosis: A Treatment Handbook. UK: John Wiley & Sons, Ltd

*Gumley, A. & Schwannauer, M. (2006). Staying Well After Psychosis: A Cognitive Interpersonal Approach to Recovery and Relapse Prevention. West
Sussex, UK: John Wiley & Sons Ltd.

*Haddock, G. & Slade, P. (Eds.) (1996). Cognitive-Behavioral Interventions with Psychotic Disorders.NY: Routledge.

*Harrop, C. & Trower, P. (2003). Why does Schizophrenia Develop at Late Adolescence?: A Cognitive-Developmental Approach to Psychosis.UK: Wiley.

Kingdon, D. G. & Turkington, D. (1994). Cognitive-Behavioral Therapy of Schizophrenia. NY: The Guilford Press.

*Kingdon, D. G. & Turkington, D. (2005). Cognitive Therapy of Schizophrenia. NY: The Guilford Press.

*Morrison, A. P. (Ed.) (2002). A Casebook of Cognitive Therapy for Psychosis. NY: Brunner-Routledge.

*Morrison, A. P., Renton, J. C., Dunn, H. et al (2004). Cognitive Therapy for Psychosis: A formulation-Based Approach. NY: Brunner-Routledge.

Perris, C. (1989). Cognitive Therapy with Schizophrenic Patients. NY: The Guilford Press.

*Perris, C. & McGorry, P. (Eds.) (1998).Cognitive Psychotherapy of Psychotic and Personality Disorders: Handbook of Theory and Practice. NY: John Wiley & Sons.

Rachman, S. (2003). The Treatment of Obsessions. UK: Oxford University Press.
(This volume does not address psychosis per se, but it has much to offer the clinician doing psychosis psychotherapy).

Reinecke, M. A. & Clark, D. A. (Eds.) (2004). Cognitive Therapy Across the Lifespan: Evidence and Practice. NY: Cambridge University Press. (This volume is not specifically about psychosis, but it has chapters on bipolar disorder and schizophrenia).

Homopathic Treatment (Dr. Watson does not endorse this as he has not vetting this treatment- informational)

Anecdotal evidence over the past two centuries leaves us supportive evidence in favor of using classical homeopathic therapy for people with schizophrenia (Frei & Thurneysen, 2001; Chapman et al, 1999; Davidson et al, 1997; Cook, 1992(~); Saine, 1997; Perez & Tomsko, 1994; Bohn, 1970; S., 1968; McDonough, 1965; Smith, 1956; Rueckert, 1949; Givens, 1905; Thacher, 1910(~); Cooley, 1898; Talcott, 1890; Worcester, 1881; Jahr, 1855; Hahnemann, 1842).

One study from India reported successful efforts of managing schizophrenia in a 1 to 8 week trial with 70 people with schizophrenia on one of two well-known remedies with psycho-tropic action in high dose. Medicines were chosen ‘classically’ by the principle of ‘totality of symptoms’ and administered in low dose (200 to 1000) homeopathic potency (Balachandran, 1976). These cases were treated in a clinical hospital setting at the Regional Research Institute between 1972 and 1974 in Kottayam, India.

Other supportive evidence comes forth through records of Homeopathic Insane Asylums (The Homeopathic World- editor, 1925). Good examples of asylums in the United States date back to the 1870’s and include the New York Homeopathic Asylum in Middletown, NY, which came under direction of a noted homeopath, Dr. S. H. Talcott, M.D.; and another asylum in Stamford, CT, which came under direction of Dr. Amos J Givens, M.D.; and a sanitarium in Cincinnati, Ohio (Grimmer, 1940; MED INV- editor, 1874).

A review of the 1901 book by Talcott “Mental diseases and their modern treatment” gives a plethora of information on homeopathic usage in mental illnesses (Talcott, 1901). Some presenting symptoms of patient cases described suggest that several people in this account have thought disorder and perceptual changes suggestive of schizophrenia.

André Saine, N.D., D.H.A.N.P., is a renowned master of classical homeopathy (Saine, 1997b). He practices in Montreal, Canada, and has noted success in managing severe cases of schizophrenia (Saine, 1997). His book on Psychiatric Patients is a testament of work, experience, and successful application of classical homeopathy with mental illness (Saine, 1997).

ORTHOMOLECULAR MEDICINE & MEGAVITAMIN THERAPY (Dr. Watson has not vetting this material).

A. Hoffer, MD, PhD, FRCP(C), Orthomolecular Treatment for Schizophrenia, Los Angeles: Keats Publishing, 1999.

Effective Non-Neuroleptic Treatment (Endorsed by Dr. Watson)

The Empathic Ward: Reality and Resistance in Mental Health Reform, by Leighton C. Whitaker, PhD, ABPP, and Arthur J. Deikman, MD, Ethical Human Psychology and Psychiatry, Vol. 11, No. 1:50-62 (2009).
Treating schizophrenia without drugs? There's good evidence for it.  Comment: PsychMinded, by Tim Carlton, April 24, 2009.

Psychosocial treatment, antipsychotic postponement, and low-dose medication strategies in first-episode psychosis: A review of the literature, by John R. Bola, Klaus Lehtinen, Johan Cullberg and Luc Ciompi, Psychosis, Vol 1, No. 1: 4-18 (2009).

Effectiveness of Long-term Psychodynamic Psychotherapy: A Meta-analysis, by Falk Leichnsenring, DSe, Sven Rabung, PhD, Journal of the American Medical Association (JAMA), Vol 300, No. 13: 1551-1565 (2008).
Factors Involved in Outcome and Recovery in Schizophrenia Patients Not on Antipsychotic Medications: A 15-Year Multifollow-Up Study, A longitudinal study of 145 patients found a40% recovery rate for those who did not take antipsychotics, versus a 5% rate for those who did, Journal of Nervous and Mental Disease, Vol 195, May, 2007, No. 5: 407-414

Five-year experience of first-episode nonaffective psychosis in open-dialogue approach: Treatment principles, follow-up outcomes, and two case studies, by Jaakko Seikkula, Jukka Aaltonen, Birgittu Alakare, Kauko Haarakangas, Jyrki Kera¨Nen, & Klaus Lehtinen, Psychotherapy Research, March 2006; 16(2): 214/228.  This study of the Open Dialogue approach in Finland that used as little neuroleptics as possible found that in a group of 42 patients, 82% did not have psychotic symptoms at the end of five years, 86% had returned to their studies or jobs, and only 14% were on disability allowance. Only 29% had ever been exposed to a neuroleptic medication at all during the five years, and only 17% were on neuroleptics at the end of five years.  Other studies of this program are:

Open Dialogue Approach:  Treatment Principles and Preliminary Results of a Two- year Follow-up on First Episode Schizophrenia, by Jaakko Seikkula, Birgitta Alakare, Jukka Aaltonen Juha Holma and Anu Rasinkangas, Ethical and Human Sciences and Services, 2003, 5(3), 163-182.
Open Dialogue in Psychosis II: A Comparison of Good and Poor Outcome Cases, by Jaakko Seikkula, Birgitta Alakare and Jukka Aaltonen, Journal of Constructivist Psychology, 14:267-284, 2001.

Recurrent Psychotic Depression Is Treatable by Psychoanalytic Therapy Without Medication, by Bertram P. Karon, PhD, Ethical Human Psychology and Psychiatry. Volume 7. Number I . SIJring 2005
Treatment of Schizophrenia Without Neuroleptics: Psychosocial Interventions Versus Neuroleptic Treatment, by Matt Irwin, Ethical Human Psychology and Psychiatry, Vol. 6, No. 2, Summer 2004.
Remember Our Heritage, by Cloe Madanes, Psychotherapy Networker, November/December 2004.  2.2 Megabytes.

Reversal of Schizophrenia Without Neuroleptics, by Matt Irwin, Howard University Hospital, Ethical Human Psychology and Psychiatry, Volume 6, Number I, Spring 2004

The Tragedy of Schizophrenia without Psychotherapy, by Bertram P. Karon, PhD, Journal of The American Academy of Psychoanalysis und Dynamic Psychiatry, 31(1), 89- 118, 2003.

Soteria and Other Alternatives to Acute Psychiatric Hospitalization A Personal and Professional Review, by Loren R. Mosher, M.D., The Journal of Nervous and Mental Disease, 187:142-149, 1999.

Cognitive Therapy for the Prevention of Psychosis in People at Ultra-High Risk: Randomised Controlled trial, by Anthony P. Morrison, Paul French, Lara Walford, Shon W. Lewis, Aoiffe Kilcommons, Joanne Green, Sophie Parker and Richard P. Bentall, British Journal of Psychiatry, 2004;185, 291-7.

The Michigan State Psychotherapy Project study compared standard medication treatment for those diagnosed with severe schizophrenia with quality controlled psychotherapy both alone and with medication as an adjunct.  The study demonstrated extremely more favorable long-term outcomes (at lower cost) for those receiving psychotherapy alone from psychotherapists with relevant training and experience.

Treatment of Acute Psychosis Without Neuroleptics:  Two-Year Outcomes from the Soteria Project by John R. Bola, Ph.D., and Loren R. Mosher, M.D., Journal of Nervous Mental Disease, 191 (2003):219-29, finds that a relationally focused therapeutic milieu with minimal use of antipsychotic drugs, rather than drug treatment in the hospital, should be a preferred treatment for persons newly diagnosed with schizophrenia spectrum disorder.
Luc Ciompi, M.D., Professor Emeritus, MD, Switzerland

The Soteria-concept. Theoretical bases and practical 13-yearexperience with a milieu-therapeutic approach of acute schizophrenia, Special lecture given at the 93 Annual Meeting of the Japanese Society of Psychiatry and Neurology, Tokyo, May 29th-31th, 1997, published in Psychiatria et Neurologia Japonica 99: 634-650, 1997.
The Concept of Affect Logic: An Integrative Psycho-Socio-Biological Approach to Understanding and Treatment of Schizophrenia, Psychiatry, Vol. 60, Summer 1997.

The Effects of Medicating or Not Medicating on the Treatment Process by Bertram P. Karon, Ph.D. discusses both the harm caused by neuroleptics and the efficacy of a psycho-dynamic process (2003).  Longer version presented at Division of Psychoanalysis (39), American Psychological Association, New York, NY, April, 2002.

Psychotherapy with "Schizophrenia": Analysis of Metaphor to Reveal Trauma and Conflict, by Richard Shulman, PhD, Co-published simultaneously in The Psychotherapy Patient (The Haworth Press, Inc.) Vol. 9, No. 3/4, 1996, pp. 75-106; and: Psychosocial Approaches to Deeply Disturbed Persons (eds: Peter R. Breggin, and E. Mark Stern) The Hawthorn Press, Inc., 1996, pp.75-106.

The Benefits of Individual Psychotherapy for People Diagnosed with Schizophrenia: A Meta-Analytic Review by William H. Gottdiener and Nick Haslam,  Ethical Human Sciences and Services, (2002) 4 (3), pp. 163-187.  This comprehensive review of the literature finds that psychotherapy is as effective as medication and that adding medication does not increase effectiveness.

How Non-Diagnostic Listening Led to Rapid "Recovery:" from Paranoid Schizophrenia:  What is Wrong With Psychiatry?   by Al Sieberts, Ph.D.  In this paper, Dr. Sieberts finds that Psychiatry lacks insight into its own behavior, invalidates constructive criticism, avoids the kind of self-examination it urges on "patients," shows little interest in accounts of successes with schizophrenic" individuals, erroneously lumps all the schizophrenias (plural) together in research studies, feels helpless and hopeless about schizophrenia, dismisses evidence that contradicts its inaccurate beliefs, and misrepresents what is known about "schizophrenia" to the public and to patients.

The Soteria Project: Twenty Five Years of Swimming Upriver, Loren R. Mosher, John R. Bola, Complexity and Change, (2000) 9: 68-74.  This paper identifies the key ingredients to Soteria's success in treating patients diagnosed with schizophrenia without or with minimal medication.

Approaches to Madness Shared by Cross-Cultural Healing Systems and Strategic Family Therapy, by Madeleine Richeport-Haley, Journal of Family Psychotherapy, Vol 9(4), 61-75, 1998.

Recovery: The Lived Experience of Rehabilitation, by Patricia E. Deegan, Ph.D., revised version of paper originally published in Psychosocial Rehabilitation Journal, 1988, 11(4), 11-19.  This very important paper describes in moving, personal terms the importance of hope in recovery.   And willingness.  And responsible action.  It also provides very important information on how to structure a program to achieve recovery.

Soteria-California and Its Successors: Therapeutic Ingredients By Loren R. Mosher M.D., suggests that the strikingly beneficial effects of the Soteria type treatment are likely due to (a) the milieu, (b) attitudes of staff and residents, (c) quality of relationships, and (d) supportive social processes.  Dr. Mosher also discusses how leadership effects the success of these programs.

Soteria Project: Final Progress Report, by Loren Mosher and Bob Vallone, 3/14/92.  (9 megabytes)
William Carpenter, Jr., "The treatment of acute schizophrenia without drugs: an investigation of some current assumptions," American Journal of Psychiatry, 134 (1977), 14-20. 

New Hope for People with Schizophrenia, Monitor on Psychology, Volume 31, No. 2, February 2000 discusses the growing evidence that people can and do recover from serious mental illness with the critical ingredient being psychosocial rehabilitation.

Psychoanalysis and Psychosis: Trends and Developments by Ann-Louise S. Silver, M.D Journal of Contemporary Psychotherapy, Vol 31, No. 1, Spring 2001.  Psychodynamic work is too often dismissed as outmoded, while no theory has been developed that rivals it in effectiveness or in ability to offer cohesive theory.

Maurice Rappaport, "Are there schizophrenics for whom drugs may be unnecessary or contraindicated?" International Pharmacopsychiatry, 13 (1978), 100-111, concludes Many un-medicated-while-in-hospital patients showed greater long-term improvement, less pathology at follow-up, fewer re-hospitalizations and better overall function in the community than patients who were given chlorpromazine while in the hospital.

Psychoanalysis and Psychosis:  Players and History in the United States, by Ann-Louise Silver M.D., Psychoanalysis and History 4(1), 2002.  In this paper, Dr. Silver outlines how psychoanalysis has had significant success in treating schizophrenia and other psychoses since the early 1900's in the United States.
Treatment at Soteria House: A Manual for the Practice of Interpersonal Phenomenology, by Loren Mosher, Robert Vallone & Alma Menn,1992.

Deinstitutionalized Residential Care for the Mentally Disordered: The Soteria House Approach, by  Holly Skodo Tilson, 1982, Grune & Stratton, Inc.  Beware: 39 Megabytes.

Susan Mathews,  “A non-neuroleptic treatment for schizophrenia: analysis of the two-year postdischarge risk of relapse,” Schizophrenia Bulletin, 5 (1979), 322-332 finds that at 12 months postdischarge, the cumulative probability of remaining well significantly favors the alternative Soteria program over the standard use of neuroleptics.

A Child Welfare Agency Project: Therapy for Families of Status Offenders, by Kenneth W. Michaels & Robert H. Green, Child Welfare, Vol LVIII. No.3:216-219 (1979).
Consumer Operated Support Programs

Traditional community resources for mental health: a report of temple healing from India, by R Raguram, A Venkateswaran, Jayashree Ramakrishna, Mitchell G Weiss, British Medical Journal, v325 p38, 6 JULY 2002

Loren Mosher, “Community residential treatment for schizophrenia: two year followup,” Hospital and Community Psychiatry, 29 (1978), 715-723 finding that two years after discharge while the alternative Soteria program patients didn't show significantly different readmission rates or symptoms, they received medications significantly less often, used less outpatient care, showed significantly better occupational levels and were more able to live independently.

Effective Psychotherapy of Chronic Schizophrenia, by Nathaniel S. Lehrman, M.D., American Journal of Psychoanalysis, (1982), Vol.42, No. 2: 121-131.  This 1982 paper presents the evidence already existing that over-reliance on neuroleptics was worsening outcomes.  In this paper Dr. Lehrman discusses how individually tailored psychotherapy can get people who have chronically suffered schizophrenia  well and back out into the community as a full member.


Here you will find important information not often known or acknowledged within the mental health community. Attached is Dr. Watson's ongoing detailed summary of research related to this topic.   IF you read down below, you will have additional information about causes of Schizophrenia-psychosis and treatments that are effective (other than psychotropic medications.)  PDF's are coming...!

Information contained herein is designed to support, not replace, the therapeutic relationship between doctor and patient. All information is kept in strict confidence, and no information, written or verbal is given out to any party what so ever without explicit written permission by our clients and patients.  Dr. Watson works under the Corporation: Associated Psychological Health Services, as a private corporation, and insured personally for his work.  He has no clinical financial ties or funding resources other than from client income.

PLEASE NOTE: Starting, adjusting or tapering and stopping psychiatric medications can be very dangerous and even life threatening.  You should not stop taking a medication without medical supervision.  Talk to your doctor about all information you may have about your mental and physical health before adjusting any medications you may be taking.  

Speak to Dr. Watson Today


"Not all answers are found in a prescription pad...    

it's elementary Dr. Watson!"