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Summer 2005

ICSPP Newsletter International Center for the Study of Psychiatry and Psychology Summer 2005 Issue SPECIAL PRECONFERENCE ISSUE Eighth Annual Conference of the International Center for the Study of Psychiatry and Psychology (ICSPP) With the collaboration of the St. John’s University Department of Psychology (Dedicated to the memory of Kevin McCready, Ph.D.) To take place in New York City, October, 7, 8, and 9, 2005 at The Sheraton LaGuardia East Hotel, 135-20 39th Avenue, Flushing, New York, 11354 SCHIZOPHRENIA and BIPOLAR DISORDER: SCIENTIFIC FACTS OR SCIENTIFIC DELUSIONS? Implications for theory and treatment Invited presenters include: Peter Breggin, M.D. Founder of ICSPP, noted author of numerous scientific publications including Toxic Psychiatry and Talking Back to Prozac; Daniel Dorman, M.D. author of  Dante’s Cure: A Journey Out of Madness; William Glasser, M.D. Internationally recognized psychiatrist and author of Reality Therapy and Choice Theory; Joseph Glenmullen, M.D. author of The Antidepressant Solution; Grace Jackson, M.D. Noted scientist and international lecturer; Bertram Karon, Ph.D.  Noted psychoanalyst and author of Psychotherapy of Schizophrenia: Treatment of Choice; Brian Koehler, M.D.; Clancy McKenzie, M.D. Director of the Integrative Psychiatry Program at Capital University of Integrative Medicine, Washington, D.C.; Dominick Riccio, Ph.D. Psychoanalyst and Executive Director, ICSPP; Ann-Louise Silver, M.D.  President of the U.S.  Chapter of The International Society for the Psychological Treatment of Schizophrenia and other Psychoses (ISPS) and Past President of the American Academy of Psychoanalysis and Dynamic Psychiatry; Laurence Simon, Ph.D.  Emeritus Professor of Psychology, CUNY, Adjunct Professor of Psychology, St. John’s University and author of Psychology, Psychotherapy, Psychoanalysis and the Politics of Human Relationships; Elliot Valenstein, Ph.D. Emeritus Professor, University of Michigan and author of Blaming the Brain; Robert Whitaker, Prize winning investigative journalist and author of Mad in America: Bad Science, Bad Medicine and the enduring Mistreatment of the Mentally Ill.        1036 Park Avenue, Suite 1B New York, NY 10028 (212) 585-3758     About the International Center for the Study of Psychiatry and Psychology. The International Center for the Study of Psychiatry and Psychology (ICSPP) is a nonprofit, 501C research and educational network of professionals and lay persons who are concerned with the impact of mental health theory and practice upon individual’s well-being, personal freedom, families, and communities. For over three decades ICSPP has been informing professionals, the media, and the public about the potential dangers of drugs, electroshock, psychosurgery, and the biological theories of psychiatry.     ICSPP is supported by donations and contributions. Officers receive no salary or other remuneration. Help us continue our work by sending a donation to ICSPP today. Schizophrenia: Medical students are taught it’s all in the genes, but are they hearing the whole story? Jonathan Leo, Ph.D. Jay Joseph, Psy.D. The abstract and Table 2 have been omitted from the present version. For these, please see the original paper: Leo, J. & Joseph, J. (2002) in Ethical Human Sciences and Services Vol. 4 No1, pp. 17-30. Requests for reprints should be sent to Jonathan Leo, Department of Anatomy, Western University of Health Sciences, 309 East Second Street, Pomona CA 91767 INTRODUCTION           The idea that schizophrenia is due at least in part to a genetic predisposition is seen as an accepted fact in modern day psychiatry.   The acceptance of this theory is not only important for how psychiatrists approach the research and treatment of schizophrenia, but also has implications for the entire field of psychiatry.  As Edward Shorter, the author of the History of Psychiatry wrote, “Among the most convincing kinds of evidence for a neural origin of major psychiatric illness would be genetic studies” (Shorter, 1997, p. 240).     The genetic theory of schizophrenia is frequently cited as evidence in favor of a genetic predisposition to other conditions; the thinking being that if schizophrenia is genetic, then depression, obsessive compulsive disorder, attention deficit disorder and a host of other DSM-IV categories must also have their roots in problematic genes. (By the expression “genetic theory of schizophrenia” we mean the view that although environmental factors might be important, genetic factors are equally if not more important.) Scientists have spent countless hours and numerous resources investigating the role of genes in certain behaviors, but a specific gene has never been found for those disorders which have no known neurochemical or neuropathological markers. In the case of schizophrenia, several scientists have reported finding a “schizophrenia gene” only to eventually retract their findings (Marshall, 1994; Sherrington et al., 1988).         When citing evidence for the genetic basis of schizophrenia, psychiatry textbooks invariably mention the twin studies and adoption studies.  As a group, these studies are one of the most frequently cited bodies of research in all of psychiatry.  It is common for neuroscience and psychiatry textbooks that discuss the importance of genetics to focus on schizophrenia, because it is thought to be best example of a “mental illness” that has a genetic component.   Unfortunately, most textbooks provide only a cursory and superficial review of the evidence supporting the genetic theory of schizophrenia.  There are two types of errors commonly found in the standard textbook discussions of this topic. The first is that some of these books misstate the actual data. The second but perhaps more egregious error is one of omission.  It is not so much what the textbooks say, but rather what they do not say. Unfortunately, most of these textbooks fail to point out the studies’ significant methodological problems, and fail to mention peer reviewed published critiques of these studies, (Boyle, 1990; Lewontin et al., 1984; Lidz and Blatt, 1983; Pam, 1995). A topic as complex as the etiology of schizophrenia should be presented to students in a fair but critical manner. Students can make sound decisions only by reviewing all the facts, and not just selected information that supports a particular viewpoint. For a first-year student who is unfamiliar with the topic, the way the material is presented will have a large impact on his or her subsequent opinions.  If students were exposed to a more in-depth review of the actual data, would the genetic theory of schizophrenia at least be open to more discussion and debate? Principles of Neural Science, often referred to as the “bible of neuroscience,” is assigned to a significant number of first-year medical and graduate students in the United States. Its authors are Eric Kandel, James Schwartz, and Thomas Jessell.  Dr. Kandel, who won the 2000 Nobel Prize in Medicine, is the author of Chapter 60: “Disorders of Thought and Volition: Schizophrenia.”   Kandel’s analysis of the scientific evidence in support of the genetic theory of schizophrenia exemplifies the problems inherent in many textbooks that cover this topic (Kandel, 2000). In light of the fact that Kandel is one of the foremost research psychiatrists in the world, it is interesting to examine the data that Kandel cites in support of his fairly strong statements concerning the etiology of schizophrenia.   It would not be an overstatement to say that within the current medical community, the overwhelming majority of practicing physicians and scientists received their introduction to the genetics of schizophrenia from this textbook.     The purpose of this review is to examine what a Nobel Prize winning psychiatrist thinks is the strongest evidence in support of the idea that genes play a major role in schizophrenia.  Kandel does not explicitly say that the environment does not play a role in schizophrenia, but in his discussion of the etiology of schizophrenia there is little mention of environmental factors.  On the contrary, he writes, “the only reliable clue as to the cause comes from the finding that schizophrenia is due in part to a genetic abnormality” (p. 1193). The three methods most frequently cited in support of genetic factors in schizophrenia are family studies, twin studies, and adoption studies. Kandel says that all three of these methodologies support the role of genetics in schizophrenia.  In this article, we examine the data that Kandel presents for each of these approaches and we will also point out the problems with each approach. FAMILY STUDIES Kandel’s Evidence. The goal of family studies is to determine if a condition is found more often in the biological families of affected persons as compared to the general population or to a control group.  According to Kandel, “the first direct evidence that genes are important in schizophrenia was provided in the 1930s by Franz Kallmann.” Kallmann, a German psychiatrist who later emigrated to the United States, noted that while the worldwide incidence of schizophrenia was approximately 1%, there were some instances in which schizophrenia was found in 15% of the family members (Kandel, 2000, p. 1193).  At first glance, the finding that schizophrenia is found to cluster in families might suggest a genetic basis for the condition.   Problems. There is little disagreement that schizophrenia (or any other psychiatric condition) runs in families. The major problem with family studies is that while these studies suggest that schizophrenia does indeed run in families, this does not mean that genetic factors are involved. Traits can cluster in families for purely environmental reasons, meaning that family studies are suggestive at best. This fact was recognized by Kandel when he wrote, “Not all conditions that run in families are necessarily genetic – wealth and poverty and habits and values also run in families” (p. 1193). On a minor note, Kallmann did not provide “the first direct evidence that genes are important.” Kallmann’s family study was published in 1938, whereas Rüdin had published a large schizophrenia family study showing similar results in 1916 (Rüdin, 1916).  In addition, schizophrenia twin studies were published in 1928 by Luxenburger (1928) and in 1934 by Rosanoff and colleagues (1934). It is also worth mentioning that even before the first family studies were conducted, both Kraepelin and Bleuler (respectively, the creators of dementia praecox and schizophrenia) believed that the condition was hereditary.  In 1899 Kraepelin wrote, “An inherited predisposition to mental disturbances was apparent in approximately seventy percent of those case in which data could be evaluated” (Quoted in Boyle 1990, p 118).  And Bleuler would write in his monograph that “heredity plays its role in the etiology of schizophrenia, but the extent and kind of its influence cannot as yet be stated” (Bleuler, 1950, p. 337). These views prompted Boyle (1990), a critic of the genetic theory, to write: Thus, before any attempt at systematic data collection was ever made, the two most prominent users of the concepts of dementia praecox and schizophrenia were disseminating the view that whatever phenomena they included under these terms were largely inherited (p. 118). Apparently, the people who created the schizophrenia concept did not need any more evidence than the behavior of their patients’ relatives to support the view that the condition was hereditary.     It is also worth mentioning that Kallmann did not make blind diagnoses and, while working in Germany under Nazi rule, he advocated the forced sterilization of people diagnosed with schizophrenia as well as their healthy relatives (Müller-Hill, 1998).  After emigrating to the United States Kallmann called for eugenic measures to eliminate the “schizophrenic genotype,” which included compulsory sterilization for “absolutely incorrigible schizophrenics who do not need hospitalization and who may be expected to propagate themselves, even out of wedlock and against medical advice” (Kallmann, 1938, p. 267) It is common for people to erroneously equate “it runs in the family” with “it’s genetic.” Kandel acknowledges the problems with the family studies and goes on to discuss other research strategies developed to disentangle the relative contributions of nature and nurture.  These strategies involve looking at two groups of people: twins and adoptees.   TWIN STUDIES Kandel’s Evidence. Twin studies are viewed as important because scientists can compare two different types of twins.  Identical (monozygotic) twins have the same genotype, while fraternal (dizygotic) twins share on average only 50% of the same genes.  If the development of a certain disease is due to heredity, then genetic researchers would expect more of the identical twins to share the disease as compared to the same-sex fraternal twins.  When discussing the twin studies, Kandel groups Kallmann’s data and the data from more recent studies together and reports a combined concordance rate of 45% for identical twins, compared to only a 15% concordance rate in fraternal twins. The data seem to provide strong evidence for a genetic basis to schizophrenia, and based on the evidence that is reported most students would probably conclude that the twin studies unequivocally prove that schizophrenia has a genetic origin.  However, it is our contention that if students were presented with a more complete discussion of the twin data, they might reach different conclusions. Problems. The first mistake that Kandel makes is to group together Kallmann and earlier researchers and cite a combined 45% concordance rate for monozygotic twins.  What should be mentioned right at the start is that Kallmann and the newer studies are actually quite different.  And more importantly, to critically minded reviewers of these studies it is these differences and not the similarities between Kallmann and the newer studies that have raised concern (Boyle, 1990; Lewontin et al., 1984; Pam, 1995).  Kallmann did not find a 45% concordance rate; he actually found a 69% rate, which he increased to 86% after factoring in an age-correction (Kallmann, 1946). It was more recent research groups that found a 40% concordance rate.  The discrepancy between Kallmann and the newer studies was addressed by Lewontin, Rose, and Kamin (1984) who pointed out in Not In Our Genes that, while Kallmann’s 86% concordance rate validated his theory of genetic predisposition (which he called “hereditary taint”) to schizophrenia, it is difficult to reconcile his findings with the more modest 40% concordance rate found in the newer studies. Thus, the fact that Kallmann found such a high concordance rate makes his data highly suspicious to Lewontin and colleagues.  They go so far as to say, “Kallmann’s data have faded from the body of acceptable evidence, but the belief for which he was largely responsible – that a genetic basis for schizophrenia has been clearly established- still remains powerful in and out of science” (pp. 212-213).  Anyone writing a review that supports the genetic theory of schizophrenia faces a dilemma with the Kallmann data: Should it be included or rejected? Kandel’s chapter is an example of the problems one faces when Kallmann’s data is included.   Kallmann aside, the validity of the twin method is based on the assumption that identical twins do not have more similar environments then fraternal twins.  The equal environment assumption (EEA) is critical for the twin method because if identical twins are treated more alike than fraternal twins, then any difference in the concordance rates between the two types of twins could be attributed to the environment.   One way of judging the validity of the EEA is to compare fraternal twins to non-twin siblings since, in terms of their genetic makeup, fraternal twins are no more alike than non-twin siblings.  Therefore, any difference in the rate of schizophrenia between fraternal twins and siblings must be due to something other than genes.  According to genetic theory, if a fraternal twin develops a condition, his or her co-twin should have just as much chance of developing it as their other brothers and sisters.  If the fraternal twins show an increased chance of developing the condition compared to the non-twin siblings, then this constitutes strong evidence of an environmental effect.  If the data show that fraternal twins do indeed share a more similar environment than the non-twin siblings, then what about the identical twins?   If the equal environment assumption is wrong and the identical twins share a more similar environment than fraternal twins, then the theoretical basis of the twin method is faulty (Jackson, 1960; Joseph, 2001c). In fact, Kandel acknowledges the importance of EEA and also the importance of the comparison between the non-twin siblings and the dizygotic twins. He defends the validity of the EEA by claiming that fraternal twins have a 15% concordance rate, which he states is the same as that found between non-identical twins and the other siblings.  This evidence would seem to support the validity of the EEA, but it is not that simple.    The data showing no difference in the concordance rate between fraternal twins and siblings are from Franz Kallmann, who reported an age-corrected fraternal “morbidity” rate of 14.7% and a full-sibling concordance rate of 14.3% (Kallmann, 1946, p. 313).  As we mentioned earlier, there are significant problems with Kallmann’s data and at this point the reader is probably asking, why even include the Kallmann data? It is suspicious, it is over five decades old, and newer data supposedly prove the genetic theory of schizophrenia anyway.  One reason for citing Kallmann in support of the EEA is because he is the only twin researcher whose data support the EEA.  In fact, every twin investigator besides Kallmann that has compared the concordance rates between fraternal twins and siblings found the rate to be higher in the fraternal twins (Fischer, 1973; Gottesman and Shields, 1972; Kringlen, 1967; Luxenburger, 1928; Slater, 1953).   It is problematic to cite Kallmann in support of the EEA and students would probably think differently about its validity if they were told the following: 1) six twin investigators have compared the concordance rates between fraternal twins and non-twin siblings; 2) the only investigator who found similar rates was Franz Kallmann; 3) the other five investigators found that the fraternal twins had a higher concordance rate compared to the non-twin siblings; and 4) two of the investigators found statistically significant differences between these two groups (See table 1).   Thus Kallmann is the odd man out here and his numbers are not a fair representation of the overall data. Furthermore, Kallmann himself reported data that is not supportive of the EEA. Contemporary reviewers almost never mention that Kallmann’s fraternal same-sex twins had a 12% concordance rate, versus a 6% rate in his fraternal opposite-sex pairs.  The difference, in fact, is statistically significant and it argues strongly against the validity of the EEA (Joseph, 1998).   It only seems fair that if we reject Kallmann’s concordance rate of 86% found in identical twins, then we should likewise reject his findings when it comes to the discussion of the fraternal twins versus siblings.  We should not pick and choose which numbers support the position we want, especially when we are presenting the material to students.  Even if the Kallmann data is not rejected, it seems fair to point out to students that his data is not typical of the twin studies. The issue becomes even more complicated because Kandel reproduces a table from Gottesman (1991) which is inconsistent with the EEA.  According to Gottesman’s table, the fraternal twin of a person diagnosed with schizophrenia has a 17% chance of receiving the diagnosis, whereas the non-twin sibling of a person diagnosed with schizophrenia has only a 9% chance (see table 2).  Thus, the very data that Kandel reproduces in his textbook demonstrates the fallacy of the EEA and contradicts his earlier statement that dizygotic twins and non-twin siblings have the same concordance rate. If fraternal twins have an increased rate of schizophrenia compared to their non-twin siblings, what might account for this?  A plausible explanation is that they share a more similar environment and emotional bond than siblings.  Furthermore, the increased rate of schizophrenia found in monozygotic twins could then be explained by their more similar environments when compared with fraternals. Since Kandel has acknowledged the importance of the equal environment assumption to the study of twins, and given the fact that the data do not support the validity of the EEA, it is evident that the schizophrenia twin studies are flawed. In summary, the methodological problems with the schizophrenia twin studies indicate that they do not provide evidence of a genetic predisposition to schizophrenia.  Kandel even mentions that “the high concordance rate in identical twins is still insufficient evidence for a genetic basis for schizophrenia” (p. 1193).  We agree with Kandel that the twin studies are insufficient and do not prove that schizophrenia is genetic.  To overcome the problems inherent in twin studies, researchers have looked at adoptees. ADOPTION STUDIES     Kandel’s Evidence. The first adoption study that Kandel cites was conducted by Leonard Heston in 1966.  According to Kandel, Heston began with adoptees who were diagnosed with schizophrenia.  Since Kandel only briefly mentions Heston’s paper we will not discuss it in detail other than to point out that Heston did not start with adoptees who were diagnosed with schizophrenia, as Kandel reports.  Heston actually started with women diagnosed with schizophrenia who had given up a child for adoption (Heston, 1966).   The most convincing evidence for Kandel (and many others) that schizophrenia  has an important genetic component comes from the work of Seymour Kety, David Rosenthal, Paul Wender, and their Danish colleagues, who examined adoptees in Denmark. There are several variations on these adoption studies, but the one that Kandel focuses on involved finding people who grew up as adopted children and were later diagnosed with a “schizophrenia spectrum disorder.” The goal was to then examine the rate of schizophrenia spectrum disorders among these adoptees’ biological family members (whom they did not grow up with) and compare that rate to the rate among the biological relatives of control adoptees, who were not diagnosed with a schizophrenia spectrum disorder. The most important papers from the Danish-American adoption studies were published in 1968 and 1975 with Seymour Kety as the lead author.  The 1968 study was based entirely on institutional records (Kety et al., 1968).  The 1975 study used the same index and control adoptees (plus one additional control adoptee) from the 1968 study but the investigators added the additional step of attempting to interview as many adoptive and biological relatives as possible (Kety et al., 1975).  Because Kandel’s chapter primarily focuses on the 1975 study, in the interest of uniformity we will primarily discuss the Kety and colleagues 1975 study. Kandel presents a table claiming that 14% of the biological relatives were diagnosed with schizophrenia, while only 3.4% of the control relatives were so diagnosed (Kandel, 2000, table 60-1, p. 1194). If this evidence is valid, and if the study is otherwise methodologically sound, it makes a strong case for the role of genes in schizophrenia. In Kandel’s words, “In addition to documenting the importance of genetic factors in schizophrenia, these studies of adoptees in whom schizophrenia developed showed that rearing does not play a major role in the disease” (p. 1194).   But is the evidence valid?     Problem #1: The widening of the schizophrenia spectrum. The only way that Kety et al. could diagnose 14% of the biological relatives with schizophrenia was to greatly broaden the definition of schizophrenia to include diagnoses such as “latent schizophrenia,” “uncertain latent schizophrenia,” and “inadequate personality.” Kandel claims that these categories are “thought to be a mild form of the disease, a nonpsychotic condition related to schizophrenia” (p. 1194).  But why should these cases be included in the overall totals when there is little evidence that chronic schizophrenia and the spectrum disorders are genetically related (Joseph, 2001a)?  Kandel also claims, on the basis of family studies, that “odd” people are found among the relatives of people diagnosed with schizophrenia: “they are socially isolated, have poor rapport with people, ramble in their speech, tend to be suspicious, have eccentric beliefs, and engage in magical thinking” (p. 1194).  The claim that “odd” people are found among the relatives of people diagnosed with schizophrenia means little, and was often made on basis of non-blind diagnoses by investigators devoted to the genetic position.  In addition, it could just as easily be the result of the negative psychological and social environments experienced by family members. The fallacy here is that correlation is seen as being directly related to genetic causation, when there is little evidence to support this view. If one limits the comparison to cases of chronic schizophrenia among the Kety et al. 1975 biological relatives, one is left with 5 cases of chronic schizophrenia among the 173 biological relatives of index adoptees (2.9%) and zero cases of chronic schizophrenia among the 174 biological relatives of control adoptees.  Yet, 5 cases of chronic schizophrenia out of a group of 173 individuals (2.9%) is not much higher then the general population rate of 1% (Joseph, 2001b).    Problem #2: Misleading statistics. To some students even a 2.9% rate among these biological relatives compared to 0% in the controls would still seem important.  This 2.9% index biological relative chronic schizophrenia rate serves as a demonstration of how statistics can be deceiving, since 4 of these 5 were half-siblings (second degree relatives).  The problem is that genetic theory would predict that first-degree relatives would have a higher rate, but Kety’s research team found precisely the opposite result. In fact, all of the major conclusions from the 1968 and 1975 studies depended on counting second-degree relatives. Benjamin (1976), one of the early critics of the adoption studies, noted that “this finding is peculiar and contradictory.  It shows, in effect, that the less consanguinity, the greater the ‘genetic’ effect.  Differences should be weakest, not strongest, in the half sibling category” (p. 1131).  Even behavior geneticists Gottesman and Shields (1976) commented that “genetic theory predicts a much higher risk for full siblings” (p.370). And finally, David Rosenthal, one of the co-authors of the Kety et al. adoption study, stated in an earlier paper that in order to “demonstrate that genes have anything to do with schizophrenia” the investigator must show that “the frequency of schizophrenia in relatives of schizophrenics [is] positively correlated with the degree of blood relationship to the schizophrenic index cases” (Rosenthal, 1974, p. 589). Kandel further complicates the issue by again citing Gottesman’s 1991 table (see table 2).  Kandel uses this table to show that data from ordinary family studies indicate that the incidence of schizophrenia is higher in first-degree relatives than among second-degree relatives. Kandel summarizes the importance of this table by saying “These data strongly support a genetic contribution to schizophrenia.”  On the one hand Kandel is acknowledging that a genetically based condition would be expected to appear more often in first-degree versus second-degree relatives, but on the other hand he fails to acknowledge that the Danish-American adoption studies found opposite results.  Kandel, like many other textbook authors who address this topic, also fails to mention the fact that in the Kety et al. 1968 study not one of the 63 biological index parents was diagnosed with chronic schizophrenia..i The fact that the statistically significant findings of the Danish-American adoption study were dependent on the inclusion of the half-sibling diagnoses and on the widening of the definition of schizophrenia is an important omission from Kandel’s presentation on the genetics of schizophrenia, and is certainly worthy of being mentioned to students. Problem #3: The lack of statistical significance. Kandel claims that the Kety et al. 1975 index versus control chronic schizophrenia biological relative difference is statistically significant (2.9% vs. 0%), but again this is not the case. In their 1975 paper Kety and colleagues simply decided not to count a control biological father who had a 1968 hospital diagnosis of chronic schizophrenia, but who had died and therefore could not be interviewed.  Nevertheless, several other non-interviewed 1968 diagnosed relatives were counted in other statistical calculations when it supported Kety and associates’ argument. The counting of this control biological father is no longer an issue, since in 1988 Kety began counting him as a 1975 chronic schizophrenia biological control relative diagnosis (Ingraham and Kety, 1988; Kety et al., 1994).  Therefore, according to Kety’s own data, the rate of chronic schizophrenia among the 1975 index versus control biological relatives is not statistically significant (2.9% vs. 0.6%; 5/173 vs. 1/174, p = .10, Fisher’s Exact Test, one-tailed). Problem #4: Alternate explanations.  Kandel says that the adoption studies show that “rearing does not play a major role.”  This is not a fact; it is an interpretation.  Alternative ways of looking at the data lead to different interpretations.  One example is that Kety and colleagues found only 16 hospital diagnoses of chronic schizophrenia out of a pool of  5,483 adoptees. This rate of 3 per 1000 is less than half the rate found in the general population.  One could therefore conclude that being reared in an adoptive home reduced the chance that a person growing up in mid-20th century Denmark would be diagnosed with schizophrenia by over 50%! This finding alone speaks powerfully for the importance of the environment. Problem #5: Discounting the environment. It is common for researchers who support the genetic theory of schizophrenia to pay very little attention to the environment.ii In the current edition of Kandel’s textbook he mentions that genetics cannot be everything but he does not discuss what other factors might be involved. However, in the previous edition (3rd) of the textbook he wrote, “Environmental influences include not only parenting and other early social interactions but also, and perhaps particularly important, perinatal injury and infections of childhood” (Kandel, 1991, p. 857).  Why Kandel has moved from his 1991 acknowledgement that the environment might be a factor to the deletion of any discussion in his current edition about environmental factors is unclear.  However, it likely has more to do with the changing patterns of thought within the field of psychiatry in general than with the findings from any one specific study.  Kandel’s decision not to discuss possible environmental influences is just one example of how far the pendulum has swung within psychiatry towards the biological model of mental illness.  For those critics who declare that this shift is based on “science” we turn our attention to the most modern adoption study. Pekka Tienari’s, Finnish Adoptive Family Study of Schizophrenia, is similar in design to Leonard Heston’s 1966 study and David Rosenthal’s 1968 and 1971 studies, but whereas these earlier studies failed to look at the family environment, Tienari has extensively looked at the adoptive family environment (Tienari, Lahti et al., 1987; Tienari et al., 2000).  According to Tienari, “The major goal of the Finnish Adoptive Family Study is to reassess genetic contributions to schizophrenia and to add measures of the adoptive family rearing environment” (Tienari, Sorri et al., 1987, p. 477).    In order to determine the role of the family environment in the etiology of schizophrenia, psychiatrists classified the adoptive families into one of five categories ranging from (1) “healthy,” to (5) “severely disturbed” (Tienari, Lahti et al., 1987, pp. 40-41). Tienari’s study has shown the importance of the family rearing environment in the etiology of schizophrenia.  In Tienari’s words, “all adoptees who had been diagnosed either as schizophrenic or paranoid had been reared in seriously disturbed adoptive families” (Tienari, Sorri et al., 1987, p. 482).   While there are several problems with the Finnish adoption study, such as the use of the schizophrenia spectrum and the evidence of selective placement of the adoptees (Joseph, 1999a, in press), there is no way to reconcile Kandel’s omission of environmental factors with Tienari’s finding that, “The combination of a schizophrenic biological mother and a seriously disturbed adoptive family was associated with a notably high likelihood of severe disturbance and a low likelihood of health in the adoptee” (Tienari et al., 1989, p. 30; for a more extensive review of the Finnish adoption study, see Joseph 1999a).  By not mentioning the Finnish adoption study in his review Kandel has left out an important contribution to the discussion. Problem #6: Ignoring the critics. Many of the problems with regard to the twin and adoption studies that we have pointed out have been addressed previously, yet the authors of psychiatry and medical textbooks typically ignore these criticisms.  As just one example, Lewontin, Rose, and Kamin’s Not in our Genes pointed out many of the problems with the twin and adoption studies, yet it’s almost never mentioned in textbooks.   Why textbook authors have ignored these critics is unclear, but one possibility is that most textbook authors are simply unaware of this literature and are too reliant on what the proponents of the genetic theory of schizophrenia have written. Another possibility is that textbook authors have indeed read the critics, but have so completely discounted what the critics are saying that the textbook authors do not even feel the need to mention them.   However, it is quite likely that readers of Kandel’s chapter would think differently about the genetic theory of schizophrenia if they were exposed to some of the criticisms.   THE HUNT FOR THE SCHIZOPHRENIA GENE Contrary to reports that often appear in the mainstream media, no one has discovered a gene for schizophrenia.  Yet, because twin and adoption studies have convinced a generation of scientists that a “schizophrenia gene” exists, the search continues.  Joseph Alper and Marvin Natowicz (1993) address the perils and pitfalls involved with searching for genes associated with and point out that genes for schizophrenia and other psychiatric conditions have been “discovered,” only to be retracted later on.  Alper and Natowicz do not believe that the failure to find genes for psychiatric disorders is due to our limited technology, but rather to the flawed belief that there is indeed a genetic basis for these conditions. In the words of Alper and Natowicz, “In view of the lack of scientific evidence for the hypothesis that there are genetic bases for mental diseases, we conclude that nonscientific beliefs play a major role in laying this hypothesis” (p. 388).      Keeping this statement in mind, it is interesting to focus on the last section of Kandel’s chapter where he discusses the ongoing search for schizophrenia genes.  In 1988 Sherrington and colleagues announced that they had found, “the first strong evidence for the involvement of a single gene in the causation of schizophrenia” (Sherrington et al, 1988 p.164).  In this study, which was published in Nature, Sherrington and colleagues reported the finding of a susceptibility locus on chromosome 5.  In the very same issue of Nature, however, there was a conflicting report by Kennedy and colleagues (1988), who did not find any susceptibility locus on chromosome 5.  Sherrington’s results were never replicated and are now frequently cited as an example of the problems involved with searching for genes associated with behaviors classified as mental illnesses (Marshall, 1994). In the current (2000) edition of Kandel’s chapter he does not mention the events surrounding either the discovery or the failure to replicate Sherrington’s findings, but instead focuses on the ongoing efforts to find the gene or genes.  However, in the third edition of the text Kandel (1991) mentioned Sherrington and colleagues discovery but did not mention Kennedy et al.’s negative findings, even though both studies were published in the same edition of Nature.  The events surrounding the enthusiasm and subsequent disappointment about chromosome 5 would appear to be a perfect opportunity for textbook authors to describe the inherent problems associated with the quest for genes associated with psychiatric conditions. CONCLUSIONS Based on the data that Kandel presents in support of the genetic theory of schizophrenia most students would probably conclude that schizophrenia has a significant genetic component. However, these students have not heard all the facts, and it is likely that if the material were presented with a more complete discussion of the evidence, students would not so quickly accept the genetic theory of schizophrenia.  Even those scientists who firmly believe that the genetic theory of schizophrenia is on solid ground would most likely agree that sound educational practice dictates a balanced discussion for such a complex topic.  After all, a sound scientific theory should be able to stand up to a complete airing of the data.   There will certainly be textbook authors who point out that in a short presentation to medical students it is impossible to present all the details of some very complicated studies, and that furthermore, it is unnecessary because the genetic theory of schizophrenia is such a well accepted fact.  For these authors,  we suggest the following sentence as an example for future chapters, The compelling evidence from the most frequently cited schizophrenia adoption study rests its case on the basis of counting spectrum disorders among index and control paternal half-siblings.   Pointing out the limitations of the adoption studies would serve two purposes. First, medical students and other health professionals would be forced to think more critically about these studies, and second, those authors who maintain the validity of the genetic theory of schizophrenia would be compelled to support the theory in light of all the facts, and not by just selectively choosing those facts which support their views.  Kandel’s conclusion that “schizophrenia is due in part to a genetic abnormality” should at least take into account the fact that the famous Kety et al. adoption studies are dependent upon spectrum disorders diagnosed among half-siblings.      It is not our intention to single out Dr. Kandel.  He is an exceptional scientist who has made great contributions to our understanding of how the brain works, particularly in the field of learning and memory, and the overwhelming majority of his textbook is outstanding.  He and his co-authors have done an excellent job of presenting the material to students.  However, his textbook chapter on schizophrenia is just one example of how psychiatry in general has uncritically accepted the genetic theory of schizophrenia.  Most undergraduate, graduate, and medical textbooks do not go into the problems with the schizophrenia twin and adoption studies and commit similar errors (Joseph, 2001d).     In light of the discrepancy between Kandel’s conclusion about the validity of the genetic theory of schizophrenia and the evidence that is presented, there are two choices for future editions of “Principles of Neuroscience” and other such textbooks.  The first choice is to present a more complete discussion of the data, especially the all-important adoption studies, and to alter the conclusion.  The second choice is to maintain the same conclusion but provide more evidence to support that conclusion.   In other words, either the conclusion or the evidence has to change, because as of now the two are not compatible.  The dilemma, for those who accept the genetic theory of schizophrenia, is to justify the theory and at the same time present a more balanced discussion of the data.  In addition, because so much of the current thinking in psychiatry is dependent upon genetic theories, and that most textbook presentations of these theories have been very one-sided, we suggest that the debate concerning the role of genetics in schizophrenia be reopened and reevaluated in a more critical manner.  We can only speculate as to how many physicians and scientists have concluded that psychiatric disorders are caused by problematic genes, after hearing only half the story. Table 1. Schizophrenia Concordance Rates for DZ Twins and Non-Twin Siblings of Schizophrenic Twins %DZ** %Siblings P* Luxenberger (1935) [a] 14.0 11.8 Slater (1953) 11.3 4.6 .007 Gottesman (1972) † 9.1 4.7 Fisher (1973) [b] 17.7 8.3 .048 Kringlen (1967) [c] 8.1 3.0 Kallmann (1946) † 14.7 14.3 *Fisher’s Exact Test, one-tailed    **DZ Same sex and opposite-sex where reported    † Age-corrected rates [a] Luxenburger’s final twin study report. Figures from Kringlen (1968, p.54) [b] Based on a strict definition of schizophrenia [c] Based on a strict definition of schizophrenia, hospitalized and registered cases. Sibling      rate is for sibs of MZs only as reported by Kringlen (1976).  In his 1976 paper, Kringlen noted that his table 57 (1967) reported incorrect cases. REFERENCES Alper, J., & Natowicz, M. R. (1993). On establishing the genetic basis of mental disease. Trends in Neuroscience,16, (10), 387-389.    Andreasen, N. (1984). The broken brain: The biological revolution in psychiatry. New York, Harper and Row.    Benjamin, L. S. (1976). A reconsideration of the Kety and associates study of genetic factors in the transmission of schizophrenia. American Journal of Psychiatry,133, 1129-1133.    Bleuler, E. (1950). Dementia praecox or the group of schizophrenias. New York, International Universities Press (originally published in 1911).    Boyle, M. (1990). Schizophrenia: A scientific delusion. New York, Routledge.    Fischer, M. (1973). Genetic and environmental factors in schizophrenia. Copenhagen, Munksgaard.    Gottesman, I. I. (1991). Schizophrenia genesis: The origins of madness. New York, Freeman.    Gottesman, I. I., & Shields, J. (1972). Schizophrenia and genetics: A twin study vantage point. New York, Academic Press.    Gottesman, I. I., & Shields, J. (1976). A critical review of recent adoption, twin, and family studies of schizophrenia: Behavioral genetics perspectives. Schizophrenia Bulletin,2, 360-401.    Heston, L. L. (1966). Psychiatric disorders in foster home reared children of schizophrenic mothers. British Journal of Psychiatry,112, 819-825.    Ingraham, L. J., & Kety, S. S. (1988). Schizophrenia spectrum disorders. In M. Tsuang and J. Simpson (Eds.), Handbook of Schizophrenia, Vol. 3: Nosology, epidemiology and genetics (pp. 117-137). New York: Elsevier Science Publishers.    Jackson, D. (1960). A critique of the literature on the genetics of schizophrenia. In D. Jackson (Ed.) The Etiology of Schizophrenia (pp. 37-87). New York: Basic Books.    Joseph, J. (1998). The equal environment assumption of the classical twin method: A critical analysis. Journal of Mind and Behavior,19, 325-358.    Joseph, J. (1999a). A critique of the Finnish adoptive family study of schizophrenia. Journal of Mind and Behavior,20, (2), 133-154.    Joseph, J. (199b). The genetic theory of schizophrenia: A critical overview. Ethical Human Sciences and Services, 1 (2), 119-125. Joseph, J. (2001a). A critique of the spectrum concept as used in the Danish-American schizophrenia adoption studies. Ethical Human Sciences and Services ,2, (3), 135-160. Joseph, J. (2001b). The Danish-American adoptees’ family studies of Kety and associates: Do they provide evidence in support of the genetic basis of schizophrenia? Genetic, Social, and General Psychology Monographs, 127, 241-278.    Joseph, J. (2001c). Don Jackson's 'A critique of the literature on the genetics of schizophrenia': A reappraisal after 40 years. Genetic, Social and General Psychology Monographs,127, (1), 27-31.    Joseph, J. (2001d). Inaccuracy and bias in textbooks reporting psychiatric research: The case of the schizophrenia adoption studies. Politics and the Life Sciences,19, (1), 89-99.    Joseph, J. (in press). The gene illusion: Genetic research in psychiatry and psychology under the microscope, Ross-on-Wye,. PCCS Books. Kallmann, F. J. (1938). The genetics of schizophrenia. New York, Augustin.    Kallmann, F. J. (1946). The genetic theory of schizophrenia: An analysis of 691 schizophrenic twin index families. American Journal of Psychiatry,103, 309-322.    Kandel, E. R. (1991). Disorders of thought: Schizophrenia. In E. R. Kandel, J. H. Schwartz and T. Jessell (Eds.), Principles of  neural science (pp. 853-868). Norwalk: Appleton and Lange.    Kandel, E. R. (2000). Disorders of thought and volition: Schizophrenia. In E. R. Kandel, J. H. Schwartz and T. M. Jessell (Eds.), Principles of neural science (pp. 1188-1208). New York: McGraw-Hill.    Kennedy, J. L., Giuffra, L. A., Moises, H. W., Cavalli-Sforza, L. L., Pakstis, A. J., Kidd, J. R., Castiglione, C. M., Sjorgen, B., Wetterberg, L., & Kidd, K. K. (1988). Evidence against linkage of schizophrenia to markers on chromosome 5 in a northern Swedish pedigree. Nature ,336, 167-170.    Kety, S. S., Rosenthal, D., Schulsinger, F., & Jacobsen, B. (1975). Mental Illness in the biological and adoptive families of adopted individuals who have become schizophrenic: A preliminary report based on psychiatric interviews. In R. Fieve, D. Rosenthal and H. Brill (Eds.), Genetic Research in Psychiatry (pp. 147-165). Baltimore: Johns Hopkins University Press.    Kety, S. S., Rosenthal, D., Wender, P. H., & Schulsinger, F. (1968). The types and prevalence of mental illness in the biological and adoptive families of adopted schizophrenics. In D. Rosenthal and S. Kety (Eds.), The transmission of schizophrenia (pp. 345-362). New York: Pergamon Press.    Kety, S. S., Wender, P. H., Jacobsen, B., Ingraham, L., Jansson, L., Faber, B., & Kinney, D. (1994). Mental illness in the biological and adoptive relatives of schizophrenic adoptees. Archives of General Psychiatry,51, 442-455.    Kringlen, E. (1967). Heredity and environment in the functional psychoses: Case histories. Oslo, Universitetsforlaget.    Kringlen, E. (1968). An epidemiological-clinical twin study on schizophrenia. In D. Rosenthal and S. Kety (Eds.), The transmission of schizophrenia (pp. 49-63). New York: Pergamon Press.    Kringlen, E. (1976). Twins-still our best method. Schizophrenia Bulletin, 2, 429-433. Lewontin, R. C., Rose, S., & Kamin, L. J. (1984). Not in our genes. New York, Pantheon.    Lidz, T., & Blatt, S. (1983). Critique of the Danish-American studies of biological and adaptive relatives of adoptees who became schizophrenic. American Journal of Psychiatry,140, 426-434.    Luxenburger, H. (1928). Vorläufiger bericht über psychiatricshe sereinuntersuchungen an zwillingen [Provincial report on a psychiatric investigation of a series of twins]. Zeitschrift fur die Gesamte Neurologie und Psychiatrie,116, 297-347.    Marshall, E. (1994). Highs and lows on the research roller coaster. Science, 264, 1693-1695.    Müller-Hill, B. (1998). Murderous science. Plainview, NY, Cold Spring Harbor Laboratory Press.    Pam, A. (1995). Biological psychiatry. In A. Pam and C. Ross(Eds.), Pseudoscience in biological psychiatry: Blaming the body (pp. 7-84). New York: John Wiley and Sons.    Rosanoff, A., Handy, L., Plesset, I., & Brush, S. (1934). The etiology of so-called schizophrenic psychoses. American Journal of Psychiatry,91, 247-286.    Rosenthal, D. (1974). The genetics of schizophrenia. In S. Arieti and R. Brody (Eds.), American Handbook of Psychiatry (pp. 558-600). New York: Basic Books.    Rosenthal, D., Wender, P. H., Kety, S. S., Schulsinger, F., Welner, J., & Ostergaard, L. (1968). Schizophrenics' offspring reared in adoptive homes. In D. Rosenthal and S. Kety (Eds.), The transmission of schizophrenia: Proceedings of the second research conference of the foundations' fund for research in psychiatry, Dorado, Puerto Rico, 26 June to 1 July 1967 (pp. 377-391). New York: Pergamon Press.    Rosenthal, D., Wender, P. H., Kety, S. S., Welner, J., & Schulsinger, F. (1971). The adopted-away offspring of schizophrenics. American Journal of Psychiatry,128, 307-311. Rüdin, E. (1916). Zur Verebung und Neuentstehung dep Dementia praecox. Berlin, Spinger Verlag OHG.    Sherrington, R., Brynjolfsson, J., Petursson, H., Potter, M., Duddleston, K., Barraclough, B., Wasmuth, J., Dobbs, M., & Gurling, H. (1988). Localization of a susceptibility locus for schizophrenia on chromosome 5. Nature,336, 164-167.    Shorter, E. (1997). A history of psychiatry. New York, John Wiley and Sons.    Slater, E. (1953). Psychotic and neurotic illnesses in twins. Medical Research Council Special Report Series No. 278. London, Her Majesty's Stationary Office.    Tienari, P., Lahti, I., Sorri, A., Naarala, M., Moring, J., & Wahlberg, K. E. (1989). The Finnish adoptive family study of schizophrenia: Possible joint effects of genetic vulnerability and family environment. British Journal of Psychiatry,155, (suppl. 5), 29-32. Tienari, P., Lahti, I., Sorri, A., Naarala, M., Wahlberg, K., Moring, J., & Pohjola, J. (1987). The Finnish adoptive family study of schizophrenia: Possible joint effects of genetic vulnerability and family interaction. In K. Halweg and M. Goldstein (Eds.), Understanding major mental disorder: The contribution of family interaction research (pp. 33-54). New York: Family Process Press.    Tienari, P., Sorri, A., Lahti, I., Naarala, M., Wahlberg, K., Moring, J., Pohjola, J., & Wynne, L. (1987). Genetic and psychosocial factors in schizophrenia: The Finnish adoptive family study. Schizophrenia Bulletin,13, 477-484.    Tienari, P., Wynne, L. C., Moring, J., Läsky, K., Nieminen, P., Sorri, A., Lahti, I., Wahlberg, K. E., Naarala, M., Kurki-Suonio, K., Saarento, O., Koistinen, P., Tarvainen, T., Hakko, H., & Miettunen, J. (2000). Finish-Adoptive Family Study: Sample selection and adoptee DSM-III-R diagnoses. Acta Psychiatrica Scandinavica,101, 433-443. Dante’s Cure: A Journey Out of Madness By Daniel Dorman, MD Other Press, New York 2004 True to its title, Dante’s Cure is the story of a young woman’s passage through hell – the hell of schizophrenia.    Narrated by veteran psychiatrist Daniel Dorman, the book chronicles the evolution of one of his first patients, Catherine Penney (Dante).  It follows her descent into anorexia and psychosis; her work in a medication-free, psychotherapeutic endeavor spanning seven years; and her triumph in claiming a strong identity which now inspires others as a healer, community leader, and lecturer.   As a neuropharmacology researcher and psychiatrist, at odds with the reductionism and interventions which have come to dominate a field ostensibly (but no longer objectively) devoted to Psyche, I read Dorman’s  book from the combined perspective of  both cheerleader (rooting for Catherine) and rival  (testing my powers of  observation, formulation, and treatment against the young Dorman).  I celebrated each of their victories, however small or fleeting.  I struggled beneath the weight of Catherine’s recalcitrant “symptoms” and the incremental pace of her recovery and individuation.  Written twenty-seven years after the treatment ended, Dorman begins the story in the fall of 1967.   We meet 17 year old Catherine Penney as she starts her senior year of high school amidst a backdrop of  familial crises that are neither sanitized nor concealed.  We glimpse the internal and external events important to a withdrawing teen who first teeters on the brink of self-starvation, then plunges over a precipice into the darkness of social withdrawal and persecutory hallucinations. Believing that all symptoms have meaning, and that the discovery of this meaning is central to the task of healing, Dorman collects the details of Catherine’s biography with the attention of an artist.  That understanding depends upon such knowledge is the key to his creative work, and we follow Dorman’s attempts to view the world through Catherine’s eyes in order to discern the adaptive functions of her dietary rituals and voices. What drives a teenager into a state of self-abnegation and catatonia ?  Dorman presents a smorgasbord of clues for his detective readers to follow: the death of Catherine’s  father, who dies in combat when she is just nine months old.  The daily crying of a depressed and overwhelmed mother, who loses this first husband when she is two months pregnant with her next child.  The doting affection of a paternal grandfather who favors Catherine to her younger sister and keeps her crib at his bedside.  The domineering aspects of a paternal grandmother who raises Catherine and her sibling while their emotionally distant mother is busy with factory work.  The arrival of an alcoholic stepfather when Catherine is six.  The uprooting from Southern California  as the re-created Marine Corps family assumes an itinerant lifestyle. The stepfather’s occasional violence and steady emotional abuse, whose running commentary criticizes Catherine’s behavior and appearance.  The deaths of the beloved grandfather and a schoolmate, one year before the onset of symptoms. Dorman’s point in furnishing these details is not to assign blame in a condemnatory fashion, but to humanize the psychotic process as an understandable outgrowth of forces which are sufficient to hijack the fragile process of self-formation.  Faced with the suffocating pressures of a symbiotic maternal fusion; the acerbic commentary of a rejecting father-substitute; and the intolerable permanence of the fresh separation from her most significant source of validation, Dorman suggests the possibility that  any identity – even a temporarily schizophrenic identity -- could be an attractive and viable means of coping. Vivid passages describe Catherine’s experiences as a patient.  There is a chilling depiction of her first hospitalization at age 18, during which she is wired for an EEG and then punctured for a pneumoencephalogram – the 1968 equivalent of today’s high tech methods of scanning the brain.  When her neurologist concludes that there is no organic cause for her hallucinations, Catherine is delivered into the hands of a psychiatrist who barely speaks to her.  This physician reflexively places her on the schizophrenia elixir of the day (Thorazine) with largely negative results.  Equally cold and painful are the reactions of family and friends, who seem sincere in wanting to help but who also seem oblivious to the traumatizing aspects of a sterile form of psychiatry which labels, medicates, and departs. Catherine spends approximately eight months on antipsychotic drugs (Thorazine alone; then Thorazine and Stelazine, provided to her by the same non-speaking doctor who presides over her non-care in the initial hospitalization).  During this time, she remains deeply psychotic and anorexic.  Fortunately, there are some health care providers who listen.   At the urging of a compassionate group therapist, Catherine is ultimately referred to UCLA.  In the fall of 1969, she becomes a patient of first year resident Dan Dorman.  Their psychotherapeutic relationship persists through three years of hospitalization, and four more years of outpatient care.  Conducted entirely without medication, Catherine’s treatment process is not without setbacks and mistakes.  However, their mutual capacity to endure the anxieties of intense work, slow change, and each other’s imperfections culminates in Catherine’s full recovery at age twenty-six. Characterizing the process of Catherine’s transformation retrospectively, Dorman himself emphasizes three main phases.  I will embellish these distinctions with some reflections of my own.  First, there is the stage of Catherine’s infantile (fetal?) regression [not eating, not talking, not walking, not bathing] during which her therapist reflects back to her the disavowed “good” parts of her Self.  This process of reflection allows Catherine to gradually internalize an identity that is not wholly evil.  In this phase, we can imagine many transferential roles for Dorman, but one with particular salience for me is the role of surrogate grandfather – filling the void that occurred with that relative’s death just one year before Catherine’s breakdown.  Another critical aspect of this early phase is Catherine’s decision to close her eyes.  That meaningful event occurs at the one year mark in therapy, symbolic of something she may have done (or may have wanted to do) around the chronological age of twelve months (not wanting to “see” the reality of her father’s death in Korea). Next, there is Catherine’s gradual thawing between therapy years two and five.  During this phase, she opens her eyes (August 1972) and starts to feel her body again. She begins to externalize (verbalize) her auditory hallucinations – a development which Dorman appreciates as the reclaiming of her previously projected feelings.  She moves to her own apartment (February 1973).   She experiences the total resolution of hallucinations (October 1973).   She resumes a more normal diet  (November 1973) and encounters her first menstrual period in seven years (winter 1973).  One year later, Catherine worries about the possibility that a continuing reliance upon her psychotherapist might compel her to assume a sick role in perpetuity.  Dorman intuits her need to assume more control and to view him as less than omnipotent.  They reduce the frequency of their work together to three days a week  (perhaps a therapeutic recapitulation of rapprochement, as Catherine takes her first true steps of partial separation) and carry this schedule through to a successful termination of therapy in spring 1976.  Third, there is the consolidation of Catherine’s identity -- particularly in the last two years of therapy, and even more so in the years which follow.  Proving that there is life beyond mental catastrophe, Dorman  recounts some of the highlights of Catherine’s post-therapy maturation.  There is a description of her brief move to Hawaii (site of mom’s courtship to her second husband, and Catherine’s second childhood home). This leads to a ten-year relationship with an exploitative military consultant whom she first meets there.  The relationship recalls the abuses of Catherine’s stepfather, and suggests the possible workings of still extant mechanisms (unconscious) connecting Catherine to her mother. Interspersed in the story of sequential romances is Dorman’s respectful unfolding of Catherine’s occupational achievements:  official licensure as a psych tech in 1978; completion of nursing pre-requisites in 1982;  and graduation from college with an RN degree in 1984. There is a gratifying description of Catherine’s heroic efforts in multiple facilities, where she informs fellow staffers and more than a few psychiatrists about hazards  (such as medication allergies) and violations (such as mendacious charting).  In quite a few cases, the failure of others to heed her warnings leads to serious crises and at least one death.  For her efforts, Catherine is repeatedly censured.  She is creatively terminated from one job in Palm Springs.  To her credit, she uses these experiences as a stimulus for spiritual growth, and as a springboard to her current activities as an advocate for consumers of mental health care.  Readers may wonder why this story was written, or how its message might apply to their situation today.  For the psychotherapist, there is the unique opportunity to comprehend a patient’s internal experience of psychosis, and the felt-sense (to use Gendlin’s language) of that phenomenon’s eventual decay.  For the patient, there is the rare opportunity to witness the possibilities of hope, perseverance, and a therapeutic collaboration which does not hurry the blossoming of Psyche in its own time. Most remarkable in this story is the fact that Dorman, even as a resident, eschews the dogma of most trainers and peers.  Conceptualizing madness as a mutable state of being, present to some degree in us all, he rejects the Kraepelinian view of schizophrenia as organic neuropathology.  Consequently, he refuses Catherine’s early requests for medication:      “…while the drug might modify [her] behavior [it] would not help her Soul.” He elaborates: “the problem is not the use of the drugs but what the use of the drugs means.   Declaring that someone has a disease of the mind that requires treatment with drugs is to tell her that she has a permanent and profound flaw, and that she will never rejoin humanity…[I]f Catherine were one of ‘us,’ simply human, then she should respond to a human touch. I had to find out.”  And find out, he did.  As the recipient of that metaphorical touch, Catherine developed similar ideas about the elements of care which she now regards as essential:     “If the doctor doesn’t trust himself, he is going to rely on something outside himself, and tranquillizers seem to be the answer.  The last thing a person needs it to have the doctor go along or initiate a false solution …  If I had received drugs I might have gotten temporarily out of my catatonic state, but I’d have been back there sooner or later.  I’ve seen patients leave the hospital, then go off their tranquillizers.  The decrease in anxiety wasn’t initiated by the patient, so when he goes off his [medication], his pain comes back and he still doesn’t know how to cope, except by going back on the drug.  I think that is demeaning.” Commenting on the time involved in her own treatment process: “The time and effort needs to be taken to get down to the crux of the matter, even though it takes a long time, because in the long run, a lot of time is wasted if the proper thing isn’t done…If the doctor is smart, he will keep on with someone even though he feels he’s not getting anywhere.  When I was in the hospital, and afterwards, I was not aware of all the little changes that were occurring…People do not suddenly give up their defenses or protections.  They are given up little by little, and one day you don’t need them anymore. “…A person has to develop the tools to face up to himself.  The struggle is the way out.  If you eliminate the suffering, you eliminate the awareness of what has to be done.  Drugs kill the creative part of the person, the part that has the ability to overcome.  The doctor thinks he’s getting the person out of pain.  I think that is bullshit.  People miss finding out what resources they have inside them.” These commentaries are heretical in today’s climate, which emphasizes the use of quick fixes according to a medical model of brain disease.  As the results of those methods (pills, voltage, or modified lobotomy)  have typically been superficial, transient, or disabling, the enduring hell in this tale appears to be a cultural and professional delusion for which guidance is still required.  One can only hope that Dorman and Penney will spread their message widely and quickly.  Another Dante needs their cure.           --     Grace E. Jackson, MD   International Center for the Study of Psychiatry and Psychology Now Available on DVD 15% off for ICSPP Members   The 2003 Seminar Conference TREATING THE DIFFICULT CHILD: ADHD, BIPOLAR AND OTHER DIAGNOSES: CHALLENGING THE STATUS QUO WIYH SOLUTION BASED THERAPY Peter Breggin, M.D. “The Biological Basis of Childhood Disorders:The Scientific Facts” David Cohen, Ph.D. “New Research on the ADHD Drugs: A Comparative Study of Stimulants” Brian Kean, M.A. “The Dangers of Diagnosing Children: Results of the Multi-modal Treatment Approach Study” Robert Foltz, Ph.D. “Bipolar, ADHD and Conduct Disorder: The Diagnostic Dilemma.” Bruce Levine, Ph.D. “Common-Sense Solutions for Disruptive Children Without Drugs or Behavioral Manipulation.” Dominick Riccio, Ph.D. “Family Therapy: the Treatment of Choice for Working with Difficult Children.” Kevin McCready, Ph.D. Psychodynamic Therapy with Children and Families David Stein, Ph.D. “A Drug-Free Practical Program for Children Diagnosed with ADHD and Most Other Behavioral Disorders.” $100.00 for the Complete Set 2004 CONFERENCE CRITIQUING DISEASE MODELS OF PSYCHOSOCIAL DISTRESS AND IMPLEMENTING PSYCHOSOCIAL THEORIES AND INTERVENTIONS Vera Sharav Screening for mental illness: The merger of eugenics and the drug industry.                            David Healy, M.D. Manufacturing consensus in psychopharmocology: the end of psychiatry as a  Science? 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Breggin, MD                                                                               Kevin McCready, Ph.D                                                                            Loren Mosher, MD                                                                            Tony Stanton, MD Children In Distress: ADHD & Other Diagnoses                                                      Presenters:           Peter Breggin, MD                                                                                    Ron Hopson, Ph.D. Working With Very Disturbed & Traumatized Children                                                      Presenter:            Tony Stanton, M.D. What Is Wrong With Psychiatric Diagnoses: Biopsychiatry & The DSM   Presenter:              Paula Caplan, Ph.D.         Drugs In Psychiatry As A Socio-Cultural Phenomenon                                                      Presenter:              David Cohen, Ph.D  Why We Shouldn’t Label Our Children ADHD or Learning Disabled                                                                                                                               Presenters:             Gerald Coles, Ph.D.                                                                                       David Keirsey, Ph.D.                             Psychotherapy Vs. Drug Therapy With Children                                                       Presenter:             William Glasser, MD                                                       New Legislation, Children, and Medication Abuses                                                        Presenter:             Hon.. Marion Crecco And They Call It Help:  How Psychiatry Has Failed Our Children                                                        Presenter:             Louise Armstrong, Ph.D. Reclaiming Our Children                                                        Presenters:            Peter R. Breggin, MD                                                                                        Jake Johnson,Ed.D.     $200.00 for the Complete Set ICSPP DVD Order Form DVDs sold only in complete sets Send order form with check or credit card information to: ICSPP Conference DVD Dominick Riccio, Ph.D. 1036 Park Avenue, Suite 1B New York, NY 10028 Name:_____________________________________________________ Address:_____________________________________________________ City:______________________________State:__________Zip:________ Telephone:___________________________________________________ Credit card: Visa___ Mastercard___American Express___Discover____ Credit card #______________________________________________ Expiration date: MM/YY____/____ ORDER: Quantity______2004 Conference x $200.00 = ___________ Quantity______2003 Conference x $100.00 = ___________ Quantity______2000 Conference x $200.00 = ___________                         Total   = ___________ Less 15% ICSPP paid member discount     = -___________ Add $10.00 shipping and handling            +  $10.00                Final total due        = ____________ OVER THREE DECADES OF ICSPP ACCOMPLISHMENTS Stopping the worldwide resurgence of lobotomy and psychosurgery on adults and children, and all psychosurgery in federal and state institutions. The creation of a federal Psychosurgery Commission by Congress (1970's) Alerting professionals to the dangers of tardive dyskinesia in children (1983). Tardive dyskinesia is a potentially devastating neurological disorder caused by neuroleptic or antipsychotic drugs. Alerting professionals to the dangers of dementia produced by long-term neuroleptic drug use (1983). Motivating the FDA to force the drug companies to put a new class warning of tardive dyskinesia on their labels for neuroleptic drugs (1985). The withdrawal of a large multi-agency federal program to perform dangerous invasive experiments in inner-city kids in search of supposed genetic and biochemical causes of violence (the violence initiative) (early 1990's). The initial cancellation and later modification of a potentially racist federally sponsored conference on the genetics of violence (early 1990's). Alerting the profession to danger of down-regulation and dangerous withdrawal reactions from the new SSRI antidepressants such as Prozac, Zoloft, and Paxil (1992-4). Monitoring, and at times modifying or stopping unethical, hazardous experimental research on children (1973-present). Encouraging that NIH Consensus Development Conference on Diagnosis and Treatment of Attention Deficit Hyperactivity Disorder to raise serious concerns about "ADHD" and stimulants for children. While each of these critiques and reform projects was initially considered highly controversial, and while each was frequently opposed by organized psychiatry, most are now widely accepted as rational, ethical, and scientific. For example, Psychosurgery is no longer widely practiced and not at all in state or federal institutions or on children in the United States; the multi-agency federal program aimed at using invasive biological procedures on inner-city children has been disbanded; the conference on the genetics of violence was delayed and then vastly modified; all experts now recognize the dangers of tardive dyskinesia in children; many researchers have confirmed that the neuroleptic drugs produce dementia, and experienced doctors now recognize the potential for dangerous withdrawal effects from the SSRIs.     Become a member by mailing a $25 check or money order (U.S. funds) ($35 U.S. dollars if mailing address is international). Check or money order should be made out to ICSPP. An additional tax-deductible donation can be added, and would be deeply appreciated. Your Donations to ICSPP help!     Your membership in ICSPP covers the expense of producing four newsletters per annum and other mailings, and helps us to continue to respond to the hundreds of information queries we receive from the public, the media, and concerned professionals. ICSPP owns and edits Ethical Human Psychology and Psychiatry published by Springer Publishing. A subscription to EHPP is $52.00 and can be ordered by clicking on “Journal” on our website (www.icspp.org). However, if you subscribe simultaneously with your dues payment the total of dues and subscription is $90.00 ($110.00 outside of the USA), a savings of $12.00. EHPP is vital both to those who seek to read, write, and publish on issues critical to institutional psychiatry as well as to the life of ICSPP as a scientific and educational institution. If paying by check please indicate that your payment is for both dues and subscription as well as any donation you care to make. Thank you.      General members receive the newsletter and the satisfaction of supporting mental health reform efforts for children, elders, racial and ethnic minorities, and other vulnerable populations. Members also receive a discount on the journal, Ethical Human Sciences and Services.     We are a volunteer organization with no officers receiving salaries or other financial benefits.     Become a general member by mailing a $50 dollar check or money order (U.S. funds) (60 U.S. dollars if address is international). Check or money order should be made out to ICSPP. International Center for the Study of Psychiatry and Psychology 1036 Park Avenue, Suite 1B New York NY 10028 Telephone: (212) 861-7400 Join US. Become a member of ICSPP today! ICSPP is a nonprofit 501 C3 organization. Name___________________________________________________________________ Title_________________Organization_______________________________________ Address________________________________________________________________ Address________________________________________________________________ City______________ State___________________________ Zip Code_____________ Country___________________________ E-mail_______________________________ Telephone_______________________________________________________________ Mail form and check to Robert Sliclen, 450 Washington Ave. TWP of Washington, New Jersey, 07676-4031 ICSPP Offices and Directors around the U.S. and the World International & North American Offices Peter R. Breggin, MD. Founder and Director Emeritus. Intl. Executive Director Emeritus, Advisory Council Member Ginger Ross Breggin The Breggin’s address: 101 East State Street, PBM 112 Ithaca, NY 14850-5543 (607) 272-5328 International Executive Director Dominick Riccio, Ph.D. 1036 Park Avenue, Suite 1B New York, NY 10028 (212) 861-7400 United States regional Director Lloyd Ross, Ph.D. 27 North Broad Street Ridgewood, New Jersey 07450 Phone: (201) 445-0280 Email: Lloydross1@worldnet.att.net  Newsletter Editor Laurence Simon, Ph.D. 2717 Belle Road, Bellmore, NY 11710 516-826-8860 lrsimon@optonline.net Director of Communications Andrew Levine, CSW 267 N. Central Park Avenue White Plains, NY 10606 (914) 633- 1905 Director of Membership Services Robert Sliclen, Ph.D. 450 Washington Avenue Twp of Washington, NJ 07676-4031 (201) 664-2566 Editors - Ethical Human Psychology and Psychiatry: An International Journal of Critical Inquiry Jonathan Leo, Ph.D. Laurence Simon, Ph.D. For International/National membership, newsletter, advocacy, and technical information contact the international office. For regional activities contact the regional directors and watch this newsletter for announcements. CSPP Australia Brian Keen, M.A. Lecturer in Education Southern Cross University PO Box 157, Lismore, NSW, 2480 Australia Phone: (066) 203797 CSPP Belgium Philip Hennaux, M.D. Medical Director, La Piece 71 Rue Hotel Des Monnaies 1060 Bruxelles, Belgium Phone: 2-646-96-01 CSPP Switzerland Piet Westdijk, Dr.Med. [M.D.] FMH Psychiatry and Psychotherapy FMH Child Psychiatry & Child Psychotherapy Sattelgasse 4, CH_4051 Basel, Switzerland Phone: (41) 61 262 22222 CSPP South America Alberto Ferguson, M.D. Av. 82, No. 9-86, Apt. 402 Bogota, Columbia, SA. (011) (571) 636-9050 US address: 4405 N. W. 73 Avenue, Ste.051-5106 Miami, Fla. 33166-6400 Website: www.icspp.org CSPP-Southeast Barry Duncan 8611 Banyan Court, Tamarac, Fl. 33321 (954) 721-2981 USA-CSPP Four Corners Louis Wynne, Ph.D. 1420 Carlisle NE, Suite 102 Albuquerque, NM 87110 (505) 280-4400 USA-Great Lakes Robert Foltz, Psy.D. 100 S. Atkinson, Suite 203 Grayslake, Il. 60030 (847) 518-9546 DrRobertF981@aol.com USA-CSPP Mid-Atlantic David Stein, Ph.D. Longwood College, Psychology Dept. Farmville, VA 23909 (804) 395-2322 USA-CSPP New England Emmy Rainwalker 187 Merriam Hill Road Greenville, NH 03048 (603) 878-3362 emmy@emmyrainwalker.com USA-CSPP North Carolina USA-CSPP Northern California Diane Kern, Dr. Criminology, MFT Insight Center 1372 North Main Street, #207 Walnut Creek, CA 94596 (925) 943-5503   REGISTRATION FORMS Eighth Annual Conference of the International Center for the Study of Psychiatry and Psychology (ICSPP) With the collaboration of the St. John’s University Department of Psychology (Dedicated to the memory of Kevin McCready, Ph.D.) To take place in New York City, October, 7, 8, and 9, 2005 at The Sheraton LaGuardia East Hotel, 135-20 39th Avenue, Flushing, New York, 11354 SCHIZOPHRENIA and BIPOLAR DISORDER: SCIENTIFIC FACTS OR SCIENTIFIC DELUSIONS? Implications for theory and treatment For more than three decades ICSPP (www.icspp.org), a nonprofit, 501 (c) research and educational network of professionals and lay persons that has been informing professionals, media, and the public about potential dangers of biological theories and treatments in psychiatry. The ICSPP Annual conferences serve as unique thought provoking forums to exchange critical ideas about the impact of contemporary mental health ideologies on personal and community values, and to disseminate models of therapeutic intervention that disavow all coercion and the compromise of ethics, rationality and scientific principles.   Participants include mental health professionals, academics, and researchers from the educational and academic communities, the medical and social sciences, and members of the public. It is no exaggeration to state that most attendees find the annual conferences the most stimulating, useful, intellectually challenging, and friendly meetings they ever attend. The Eighth Annual Conference will be held in New York City and promises to be the best ever. TENTATIVE PROGRAM: 2005 CONFERENCE PROGRAM A THREE-DAY MULTI-DISCIPLINARY  INTERNATIONAL CONFERENCE FOR PROFESSIONALS, STUDENTS, AND THE GENERAL PUBLIC SPONSORED BY THE INTERNATIONAL CENTER FOR THE STUDY OF PSYCHIATRY AND PSYCHOLOGY, INC. The St. John’s Department of Psychology and AMEDCO, LLC. OCTOBER 7TH, 8TH AND 9TH, 2005, 8 A.M.-5 P.M. SHERATON LAGUARDIA EAST HOTEL 135-20 39TH AVENUE FLUSHING, NEW YORK 11354 Schizophrenia and Bipolar Disorder: Scientific Facts or Scientific Delusions Implications for Theory and Practice PROGRAM THIS CONFERENCE IS DEDICATED TO THE LIFE AND ACCOMPLISHMENTS OF DR. KEVIN MC CREADY                 FRIDAY, OCTOBER 7TH, 2005 7:30 A.M. – 8:30 A.M.            REGISTRATION 7:30A.M. - 8:30A.M.            COMPLEMENTARY CONTINENTAL BREAKFAST     Phoenix Ballroom MORNING SESSIONS: 8:30 A.M. – 8:45 A.M.   Welcome & Introduction: Dominick Riccio, Ph.D. Executive Director  ICSPP  and  Conference co- chair                        Laurence Simon, Ph.D. Journal and Newsletter  editor  and Conference co-chair                        Peter R. Breggin, M.D. , Founder of ICSPP, Exec. Dir. Emeritus ICSPP                                                                        Raymond DiGiuseppe, Ph.D Chair, St. John’s Department of Psychology 8:45 A.M. – 9:45 A.M. Plenary Session:      Presenter:     Brian Koehler, MD             A comprehensive Model of Schizophrenia                            9:45 A.M. – 10:45 A.M.   Plenary Session:    Presenter:        Eliott Valenstein Ph.D.                                                                    Biochemical Theories of Mental Illness: Some Hard Facts about Soft Science 10:45 A.M. – 11:00 A.M                REFRESHMENT BREAK                                     11:00 A.M. – 12:00 P.M.  Plenary Session:      Presenter:      Laurence Simon, Ph.D.                                         Abnormal Psychology Textbooks: Valid Science or Oppressive Propaganda 12noon- 1:00 P.M                                                   Presenter:              Clarence McKenzie, MD                                                                 Delayed Posttraumatic Stress Disorder from Infancy and the Two Trauma Mechanism 100 PM – 2:00 PM                                                                 Lunch Break FRIDAY, OCTOBER 8TH, 2005 AFTERNOON SESSIONS: 2:00 P.M. – 3:30 P.M.    Workshops Workshop A                    Jeffrey Lacasse, MSW  and Jonathan Leo, Ph.D:  Antidepressant Advertising: Does the Science Support the Marketing Workshop B:                    Tom Bratter Ph.D. , Ken Steiner, Ph.D., Danielle Kaufman                                                              Toxic Psychiatric Diagnosis Workshop C:                     William Glasser MD                                                          Choice Therapy                                        Ruby 3:30PM – 3:45                                                             Refreshment Break 3:45 – 4:30 Paper Sessions                                                      PRESENTATION A        Bill Andrews, MD : Working with Human Givens: New Ideas About the Management of Mental health Including Schizophrenia and Bipolar Disorder         Jade                PRESENTATIONB                                 Nathaniel Lehrman, MD: Rethinking Schizophrenia                                                PRESENTATION C        Laura Kerr, Ph.D. Depression and Mania as Narrative Disruptions: An Alternate to Medical Models of Mood Disorders                     West PRESENTATION D                                 David Stein, Ph.D.: A Cognitive/behavioral System: A Hidden, Non-Medically Based Pattern Mapping                         Ruby     PRESENTATION E        Carolyn Crowder, Ph.D. Alfred Adler’s Psychodynamic View of Schizophrenia 4:30 – 5:15                                   PRESENTATION F         Toril Terkisen, RN, Ph.D. Cand.: Transforming Extraordinary Experiences into the Concept of Schizophrenia: A Case Study of a                       Norwegian Psychiatric Unit                                                                                                       West PRESENTATION G        Barry Duncan, Psy.D. : The Heroic Client: Recasting the Drama of Therapy                                          Jade PRESENTATION H                                   Elizabeth Root,MSW: Bipolar Mania Among Children’s Clinicians: A Report From the Front PRESENTATION I                                     Louis Wynne, Ph.D.: Thomas Szasz’ Gauntlet PRESENTATION J                                      Diane Kern, D.Sc.: Mind as a Self-organizing System: Implications for Treatment SATURDAY, OCTOBER 8TH, 2005 7:30 A.M. – 8:30 A.M.        COMPLEMENTARY CONTINENTAL BREAKFAST                    Phoenix 8:30 A.M. –   9:30 A.M.     Plenary Session:     Presenter: William Glassser  Ph.D.                     Treating Mental Health as a Public Health problem 9:30   A.M. – 10:30 A.M.   Plenary Session:     Presenter:  Peter Breggin, M.D.                     Current Trends in Diagnosing and Treating Bipolar Disorder in Children and Adults 10:30 A.M. – 10:45 A.M.                                     REFRESHMENT BREAK 10:45 A.M. – 11:45 A.M.   Plenary Session:     Presenter: Dominick Riccio, Ph.D.                     Why Mental Health Professionals Fail in Their Treatment of “Schizophrenic and Bipolar” Diagnosed Clients.               11:45 P.M.-12:45 P.M.       Plenary Session:       Presenter: Bertram Karon, Ph.D.                                                         Treating the Severely Disturbed Without the Luxury of Long-term Hospitalization 12:45 PM – 1:45 PM                                                                                   LUNCH                                                                                        AFTERNOON SESSIONS 1:45 P.M.– 3:15 P.M.   WORKSHOP SESSIONS Workshop I:      A Psychodynamic Approach to Suicidal Children Without Resorting to Brain Disabling Drugs East            Presenters: Lloyd Ross, Ph.D. and Abraham Matus, Psy.D.         Workshop II:           Reversal of Schizophrenia Without Neuroleptics     Phoenix                                          Presenters: Matt Irwin, MD and Bertram Karon, Ph.D.        Workshop III:           To be Announced          Presenters: Kermit Cole, Steve Coe and Jim Gottstein West 3:15 PM – 3:30 PM                     REFRESHMENT BREAK 3:35 P.M. - 4:20 P.M.      PAPER SESSIONS PRESENTATION A:                               Robert Foltz, Psy.D.: The Mistreatment of Mood Disorders in Youth                            Phoenix                                                                            PRESENTATION B:         Brian Kean, Ph.D.: Teachers as Agents for the Therapeutic State                     West         PRESENTATION C:                         Jim Gottstein, JD, Esq.: Grass Roots, Multi-Organizational Efforts in Support of Human Rights in Mental Illness East                  PRESENTATION D:          Jack Rosberg, Ph.D.:  Preparing the Schizophrenic for Treatment  Jade                       PRESENTATION E:                                Jeanne Stolzer, Ph.D.: Early Childhood Experiences and the Development of Schizophrenia: An Existential View       4:25 P.M. – 5:15 P.M. PRESENTATION F:                              Cesar Hernandez, BA: Effects of Different Frequencies of Photo-Stimulation in EEG’s Relative Power – An Alternative Treatment for Bipolar Disroder     Ruby PRESENTATION G:         Dan L. Edmunds, Ed.D. Thinking Outside the Biopsychiatric Paradigm: Treatment of the Insanity of the Mental health System Phoenix                    PRESENTATION H          Clover Smith  The Heredity/Environmental Cause, 31-year Psychiatric Exacerbation and 6-month 12 Step Cure of a Paranoid Schizphrenic     West        PRESENTATION I                           Bob Johnson, MRC Psych Changing From Drugs to Psychosocial Treatment with Dangerous Psychotic Long Term Prisoners: A Five Year Study   Jade                PRESENTATION J                           David M. Siegel JD: Involuntary Psychotropic Medication to Competence No Longer an Easy “Sell”  East     East          6:00 P.M. – 8:30 P.M.          MEMORIAL DINNER  IN HONOR OF DR. KEVIN MCCREADY:             PLEASE PURCHASE YOUR $50. TICKET IN ADVANCE. SEATING IS LIMITED                                         8:30 p.m. -12:00 P.M.            Irish Celebration of the life and accomplishments of Kevin McCready SUNDAY, 0ctober 9th, 2005 7:30 A. M. – 8:30 A.M.            COMPLEMENTARY CONTINENTAL BREAKFAST     Phoenix MORNING SESSIONS:   8:30 A.M. –   9:30 A.M.     Plenary Session:         Presenter: Ann Louise Silver, MD                 Keeping The Spirit and Philosophy of Chestnut Lodge Alive 9:30   A.M. – 10:30 A.M.   Plenary Session :     Presenter: Grace Jackson, MD                  Allostatic Loads: Exploring the Long-Term Consequences of Psychiatric Drugs                                                                         10:30 A.M. – 10:45 A.M.                                 REFRESHMENT BREAK 10:45 A.M. – 11:45 A.M.   Plenary Session :          Presenters: Daniel Dorman MD                                                                                                                              Psychosis as a Fact of the Human Condition                         11:45 A.M. – 12:45 P.M.    Plenary Session:       Presenter: Joseph Glenmullen, MD                                                                                   &nbs