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.   

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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 on Bipolar disorder and Standard Antipsychotic Medications


8. Although the public has often been told that people with Bipolar disorder will suffer with the disorder over the lifespan, studies that researched the chronicity of the disorder prior to 1955 found that is was quite rare and it was not a lifetime disorder.  There were only about 2,400 “first admissions” for Bipolar illness yearly in the United States mental hospitals.  75% of the first admission patients would recover within 12 months, and only 15% of first admission patients would become chronically ill (i.e. 70-85% had “good outcomes”). [4]  Researcher Dr. Healy researched medical records of hospitals from 1875 to 1924 and calculated the rate of what we call Bipolar Disorder only accounted for 1 in 100,000 cases.[5]  In 1968, researcher Silverman cited first admission studies on Bipolar disorder over the 1940’s, 1950’s, and 1960’s indicated the rate rose to one in 10,000 to one in 50,000; however, the prevalence (at one given time) rate rose to one in 3,000 to one in 10,000, still noting it was extremely rare.[6]  In 1931, Horatio Pollock, of the New York Dept. of Mental Hygiene studies 2,700 “manic-depressed” patients from 1909 to 1920, and noted that 50% only had a single attack and only 33% had an additional single attack over the period.[7]   Lundquist in his 1945 study of 95 manic patients indicated that 75% were “well” within 10 months; 42% became ill one more time over the course of 20 years, and 85% socially recovered.  Thus, only 8.5% were chronically ill over the lifespan.[8] Psychiatric medications were initially attempted as an intervention to quicken the rate of recovery, as NIMH head Dr. Dean Schuyler explained, with recovery rates exceeding 50% within a few months, it was difficult to “judge the efficacy of a drug, a treatment [ECT] or psychotherapy…”.  The depressive course of the illness “will run their course and terminate with virtually complete recovery without specific intervention.”[9]


Despite patients with psychosis were 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[10]. In fact, attempts to quantify D2 receptor density in vivo with PET scans have also proved inconclusive results.[11] 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.[12]  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. [13]


9. Since people struggling with psychosis have no known “chemical imbalance” in the brain, antipsychotic drugs cannot be said to work by “balancing” brain chemistry. These drugs are not like “insulin for diabetes.” They do not serve as a corrective to a known biological abnormality.  Instead, 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.[14] This thwarting of normal dopamine transmission is what causes the drugs to be so problematic in terms of their side effects.


10. Psychiatry’s belief in the necessity of using the drugs on a continual basis stems from two types of studies. 


a) First, research by the NIMH has shown that the drugs are more effective than placebo in curbing psychotic symptoms over the short term (six weeks).[15],[16]


b) Second, researchers have found that if patients abruptly quit taking antipsychotic medications, they are at high risk of relapsing. [17],[18], [19]


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 (See above footnote Cole, 1964).  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.[20]  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.[21], [22], [23]  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%.[24] 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. [25]


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.[26], [27], [28] 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.[29]

            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 antipsychotic-Dopaminergic blocking agent, particularly abruptly, it 'unmasks' the now up-regulated Dopaminergic receptors resulting in a 'tardive’ or ‘rebound’ or ‘supersensitivity’ psychosis.[30]

            Researchers have found the same is true for other categories of psychiatric medications, including antidepressant medications, such as Selective Serotonergic Reuptake Inhibitors[31],[32]. In those cases, they call the upregulation of the serotonergic system, “Tardive dysphoria”[33] and “oppositional tolerance”[34],[35].  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.” They 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.”[36]  Then, Harvard researchers observed that “prognosis for bipolar disorder was once considered relatively favorable, but contemporary findings suggest that disability and poor outcomes are prevalent.” They now note that “neuropharmacological-neurotoxic factors” might be causing “cognitive deficits in bipolar disorder patients.”[37]



IV. Research Showing that Recovery Rates are Higher for Non-Medicated Patients than for Medicated Patients (i.e. they tend to have better functioning and competency).


16. The studies cited above show that the these psychotropic medications increase the chronicity of psychotic symptoms over the long term. There are also a number of studies documenting that 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.[38], [39], [40]


b) Despite claims that medications and hospitalization are effective for treatment, in 1998 University of Cincinnati psychiatrist found that only 24% of their bipolar patients were “functionally recovered” at the end of one year.[41] 


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.[42], [43], [44], [45] In particular, Jaako Seikkula recently reported that five years after initial diagnosis, 82% of his psychotic patients are symptom-free, 86% have returned to their jobs or to school, and only 14% of his patients took and are on antipsychotic medications.[46]


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 antipsychotic 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 antipsychotic medications.[47]


f) Then in 2013, Dutch researcher Wunderink published the results of a “gold standard” randomized controlled study to assess if antipsychotic medication specifically could be leading to a worsening of outcomes.  Wunderink randomized 128 first episode psychotic patients following six months of antipsychotic 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…”.[48]


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, [49] 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 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.” [50] 


Other researchers noted this type of intervention “may be cost effective in the long run,” [51] as treatment for Schizophrenia accounts for approximately 30 percent of the 104 billion spent on mental health in the United States.[52]  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. [53]


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.” [54]


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.”[55] 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..[56] The risk of developing this possible life threatening effect from the neuroleptic or atypical medication increases with higher doses and longer duration.[57]


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.[58], [59], [60], [61], [62]


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.[63] The quality of life on conventional neuroleptics, researchers agreed, is “very poor.” [64]


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.”[65] 


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.[66], [67], [68]


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. [69]  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).[70], [71] 


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.[72] 


VI. The Research Literature on Atypical Antipsychotics


19. 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.


20. 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.”[73]


21. 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.[74], [75], [76], [77], [78] 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.”[79] 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 antipsychotic medications.[80] 


22. 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.[81]


23. 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.”[82]


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.[83]


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.[84] 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.


24. There is also more growing evidence that the antipsychotics (atypicals) may be exacerbating the problem of early death. Although the atypicals may not clamp down on dopamine transmission quite as powerfully as the old standard neuroleptics, they also block a number of other neurotransmitter systems, most notably serotonin and glutamate. As a result, they may cause a broader range of physical ailments, with diabetes and metabolic dysfunction particularly common for patients treated with Zyprexa. In a 2003 study of Irish patients, 25 of 72 patients (35%) died over a period of 7.5 years, leading the researchers to conclude that the risk of death for psychotic patients had “doubled” since the introduction of the atypical antipsychotics. [85]


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.[86]


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. [87] 


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. [88]  


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.[89]  They also noted prior meta-analysis research of 15 clinical trials, and found a 50% increase in mortality for patients taking newer antipsychotic medications[90], but that subsequent observational studies found similar mortality risks for first generation antipsychotic medications,[91] [92] [93] 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.[94] 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.


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