The Four False Pillars of the

 Biological Model of Mental Illness-

By: Ty Colbert, PhD, Edited By Toby Watson, PsyD

            

Psychiatry's claim that such dysfunctional symptoms used to diagnose someone with schizophrenia and manic depression are neurobiological in origin, i.e., they are diseases, is contraindicated by the absence of any biological means of diagnosis.  There is no blood test, no urine analysis, no cerebral spinal fluid analysis, or brain scan that can unequivocally identify a so-called schizophrenic person from a so-called normal person.  Although there are obviously valid diagnostic tests with which to identify true biological diseases such as measles, AIDS, pneumonia, diabetes, or anemia, there is absolutely no existing biological diagnostic testing procedure with which to identify any mental disorder.

 

In addition, contrary to popular belief, it is frequently admitted within the ranks of psychiatry that no conclusive evidence exists to show that any form of mental illness is biologically caused.  For example, the American Psychiatric Association (APA) states that theories “about the causes of schizophrenia abound, but research hasn’t pinpointed the origins.”¹   Nancy Andreasen, psychiatrist and former editor of the American Journal of Psychiatry states, “Schizophrenia also differs from the classic dementias in that there is no visible neuropathological markers…” ²  In a psychopathology textbook used for second-year medical students, the authors write, “psychiatry is the only medical specialty that...treats disorders without clearly known causes.”³ In a recent consensus conference sponsored by the National Institutes of Health (NIH) in November of 1998, the panel of experts concluded, “there are no data to indicate that ADHD is due to a brain malfunction.” In their report they went on to state that the same can be said for “most psychiatric disorders, including disabling diseases such as schizophrenia.”⁴  Finally this author has personally combed the 1000 page 1998 Textbook of Psychopharmacology⁵ and the 1700 page 1999 Textbook of Psychiatry,⁶ both published by the APA, and found no reference to any know cause for any mental illness.

 

The Four False Pillars of Biopsychiatry

 

Pillar #1: The Inheritance Pillar: Mental illness runs in families; therefore, mental illness must be inherited.

 

Pillar #2: The Chemical Imbalance Pillar: Medication works by correcting a chemical imbalance; therefore, mental illness must be a disease.

 

Pillar #3: The Defective Gene Pillar: Defective genes have been found for some disorders; therefore, mental illness must be a genetic disorder.

 

Pillar #4: The Brain Imaging Pillar: Evidence of a “diseased brain” can be detected using brain imaging instruments.

 

False Pillar #1: The Inheritance Pillar

 

1.  They say it tends to run in families.  Yeah, but so does religion and how I mash my potatos.

 

2.  They use Twin Studies: comparing concordance rates of (MZ) and (DZ) twins.   Thus, 100% vs 50% of gene sharing or pool.  Thus, should have much higher rate (really double) of disorder in MZ twins since they are genetically the same. The identical twin concordance is usually reported to be 50% (schizophrenia).  Thus, if one MZ twin has Dx 50% other will too.  For all MZ studies on schizo, 69% (Kallmann, 1946)¹² to 15% (Tienari, 1963/75).¹³ 

When ALL the studies are averaged, the rate is 43% (Pairwise rate).  The 50% rate was reached by using the probandwise statistical calculation method instead of the standard statistical pairwise method. 

Probandwise artificially inflates MZ concordance rates.¹⁴

 

3.  Major methodological research flaws in the earlier MZ studies.  Tienari (1963/75) and Hoffer and Pollin (1970/83)¹⁵ most reliable primarily because they did not depend on hospital records.  Hospital records skews results and end up having higher concordance rates for MZ.  Tienari rate (15%) & Hoffer & Pollin rate (18%) results in a concordance rate of only 16.5%,

 

4.  For the sake of accuracy, it does not make sense for biological researchers to average in older, less accurate studies; but they include them because they raise the concordance rate (i.e. they are the highest rates) and buttress the inheritance pillar.

 

Identical Twin Studies Vis-à-vis Fraternal Twin Studies

It is the differences in the concordance rates between MZ and DZ twins that must be examined because MZ twins share twice as many genes as DZ twins. We know that the Tienari and the Hoffer and Pollin studies showed the average MZ rate at 16.5%.  The corresponding average DZ rate is only 5%.¹⁶  Does this difference provide the evidence that is needed to declare that schizophrenia is genetic? No it does not.  In order to draw such a conclusion, the researcher(s) must first satisfy the "equal environmental assumption."  In order for the differences in concordance rates between MZ and DZ twins to be attributed to genetic influences, it must be assumed that DZ twins share as equal an environment with each other as do the MZ twins.  If not, then the concordance rate differences must be attributed in whole or in part to environmental influences. We know that MZ twins tend to share a more equal environment than do DZ twins.  Rosenthal, a genetic proponent, notes that same-sex fraternal twins are significantly more concordant than are opposite-sex (fraternal) twins because of their closer association and greater investment similarities.¹⁷  How much due to same environment can not be answered, therefore it is impossible to conclude a genetic basis from the MZ/DZ concordance rates. 

 

Adoption Studies

Because of the problem with the equal environmental assumption,  adoption studies were developed. 

In the late 1960's a group of American researchers (Kety, Rosenthal, & Wender)^18,19,20 , Yet when other researchers examined the studies, major methodological problems.  R. C. Lewontin, Steven Rose, and Leon Kamin in their book Not In Our Genes comment: ...”so obvious upon critical review...”

Theodore Lidz, “...data are untenable, distorted to support their hypothesis."²⁴

 

Biggest problem: "selective placement."  Adoption agency kids are not randomly placed.  Kids from high SES are often placed with high SES families and vice versa.  Lewontin, Rose, and Kamin affirmed= selective placement factor alone "undermines the theoretical separateness of genetic and environmental variables claimed for adoptive studies."²⁶  Hutchings and Mednick (1975) "most important limit of the adoptive method is the possibility that the adoption procedure results in selective placement."²⁷

 

 

False Pillar #2: The Chemical Imbalance Pillar

 The chemical imbalance pillar is the easiest to dissect.  Because certain drugs appear to reduce the symptoms associated with a particular mental disorder, and because these drugs affect the neurotransmitters in the brain, it is assumed that the medications work by correcting a chemical imbalance.

 

Yet no chemical imbalance has ever been found even though neuroscientists now have the technology to find imbalances if they were present.  This has also lead Peter Breggin, in his book Brain Disabling Treatments In Psychiatry, to declare that “there are no known biochemical imbalances in the brain of typical psychiatric patients."²⁸ Again, if one were to search the 1000 page 1998 Textbook of Psychopharmacology²⁹ and the 1700 page 1999 Textbook of Psychiatry,³⁰ it would soon be obvious to the reader that no chemical imbalances have been found for any so-called mental illness.  Such results led Dr. William Wirshing, a researcher and professor of psychiatry at UCLA, to state to a room full of psychiatrists that “we have been lying to everyone for years concerning the chemical imbalance model.”³¹  No one in the audience challenged him.

 

Since the assertion of a chemical imbalance is just a model, are there other equally valid explanations for the apparent medication-induced reduction of symptoms?  Of course! The main alternative to the chemical imbalance model is that psychiatric drugs "work" by disabling the brain.  In fact, the research evidence leads to the inference that the brain-disabling model has much more validity.

 

Both Peter Breggin³² and Joseph Wu,³³ a leading researcher at the University of California at Irvine, state that neuroleptics (antipsychotic medications prescribed for schizophrenia) act as "frontal lobotomies." Surgical lobotomists sever nerve fibers that connect the frontal lobes to the thalamus, thereby stopping the flow of messages in the brain.  Neuroleptics act as frontal lobotomies because they inhibit the flow of messages in the brain by interfering with the normal action of the neurotransmitter dopamine.

 

Patients using neuroleptics confirm this point.  One ex-patient puts it this way: "When they injected me with Prolixin, I felt everything that was me-my ability to think, my ability to remember, and so forth--begin to dissolve."  Another ex-patient says "It is very hard to describe the effect of this drug [Prolixin] and others like it.  That's why we use strange words like 'zombie."'

 

The more you listen to people who have taken these drugs, the more you realize that their brains have been immobilized, not chemically balanced.  One of many who has experienced taking antipsychotic medication and written about his experiences is Mark Vonnegut, author of The Eden Express:

 

The side effects were bad enough, but I liked what the drug was supposed to do even less.  It’s supposed to keep you calm, dull, uninterested and uninteresting…What the drug is supposed to do is keep away the hallucinations.  What I think it does is just fog up your mind so badly you don’t notice the hallucinations or much else.³⁴

 

Peter Sterling, a researcher in the area of neurology, also believes that neuroleptics have a lobotomizing effect:

 The blunting of conscious motivation and the inability to solve problems under the influence of chlorpromazine resembles nothing so much as the effects of frontal lobotomy.... Research has suggested that lobotomies and chemicals like chlorpromazine may cause their effects in the same way, by disrupting the activity of the neurochemical dopamine.  At any rate, a psychiatrist would be hard-put to distinguish a lobotomized patient from one treated with chlorpromazine.³⁵

 

Perhaps the most important challenge to the chemical imbalance model is that psychiatric drugs--whether neuroleptics, lithium (prescribed to calm manics), or antidepressant medications--equally affect animals and "normal" people as they do so-called chemically imbalanced people.  Lithium, which subdues a manic, subdues normal people too.³⁶ It was discovered because of its sedating effect on guinea pigs.³⁷  Are animals and normal people also chemically imbalanced?

 

Ritalin is given to millions of children diagnosed as ADHD to enable them to sit quietly in their chairs and do routine work.  What happens when you give Ritalin to rats?  Instead of wandering around their cages investigating and exploring in natural curious ways, they stay put and do repetitive, stereotypic tasks.³⁸ Ritalin clearly affects children and rats in much the same way.  Does Ritalin correct a chemical imbalance in rats?

 

Alcohol is used by millions to reduce anxiety at business luncheons, parties, and receptions.  Many psychiatrists maintain that anxiety is due to a chemical imbalance for which they prescribe anxiolytics.  Because alcohol reduces anxiety in most people, should we infer the presence of a chemical imbalance in them? No! Alcohol "works" by disabling the brain.

 

The truth is that there is less and less evidence to support the effectiveness of any psychiatric drug.  Studies now show that cognitive therapy alone is as effective as either antidepressant drug therapy alone or the combination of cognitive therapy and antidepressant drug therapy.^39,40  After 6,000 published studies over a 30-year period, no positive statement can be made about the long-term efficacy of prescription stimulants such as Ritalin regarding children and adolescents.⁴¹

 

Concordantly, Fisher and Fisher reviewed many studies of children and adolescents regarding antidepressant medications.  Their 1997 published conclusion is that there is absolutely no therapeutic justification for prescribing such drugs to them.⁴² In a similar review that was published between 1985 and 1994, Sommers-Flanagan and Sommers-Flanagan concluded likewise.⁴³

 

Perhaps the most revealing and damaging study is a meta-analysis of all the outcome literature concerning the treatment of schizophrenia over the last 100 years.⁴⁴  Prior to 1920, when no specific treatment was available for psychosis or schizophrenia, the improvement rate was 27.6%.  In the 1930's when convulsive therapies (insulin coma and electroshock) were introduced, the improvement rate rose to 34.9%.  However, since the introduction of the most advanced antipsychotic drug treatments in 1986, the improvement rate has increased only another 1.5% to 36.4%.  To make it crystal clear, there has been no significant improvement in outcomes over the last 100 years either through the use of convulsive therapies or medications.

 

No chemical imbalance has ever been found, nor is there any evidence to prove that psychiatric drugs correct a chemical imbalance.  Considerable evidence does exist, however, to support the "brain disabling model." Modern biopsychiatry is not curing mental illness; it is disabling brains to control behaviors and emotions labeled as diseases.

 

 

False Pillar #3: The Defective Gene Pillar

 

I spoke with the department head of a Ph.D. program in clinical psychology at a well-known accredited university.  I was discussing with him the lack of any substantial evidence to support the medical model.  He responded by saying that he had just seen an article in the Los Angeles Times that reported that scientists had located a gene for schizophrenia.

 

His response represents a deplorable situation from at least two perspectives.  It illustrates that both the professional and the lay communities are relying on inadequate sources for information about mental illness, i.e., the local news media and lectures given by "experts" who are most often compensated by pharmaceutical companies to conduct research with a particular end point in mind.  The other regrettable aspect is that the research to which he was referring did not find a gene but only a marker.  There is a big difference.

 

As a matter of fact, no defective gene has ever been found with respect to any mental disorder even though almost the entire human genome has been searched.  What researchers are finding are markers, not genes.  Markers indicate only the possibility that a gene exists.

 

Genes are nearly impossible to find directly.  Researchers must first locate a marker that they suspect resides near a gene for a particular disorder.  For example, let's say a researcher finds a group of blood-related people (a kindred) with a genetic defect which results in four fingers instead of five.  If the researcher recognizes that the relatives with four fingers also have a much higher incidence of schizophrenia, then he might suspect that the gene causing the four-finger mutation may be close to the gene for schizophrenia.  The four-finger gene then represents a marker for a possible gene for schizophrenia.  In the process of matching markers and genes, researchers calculate probability scores.  A probability score or LOD score (logarithm of the odds) of 3 is the same as 10³ or chances of 1 in 1000 that a marker has not located a gene.  When an LOD score is 3 or greater, a study is considered publishable.

 

So when a study is published, the authors are not saying that a gene has been found; they are only saying that a marker has been found with a specific probability that a gene will be located.  A published study affirming the location of a marker does not mean that a gene has been identified, will be identified, or even that such a gene exists.

 

Chromosomal markers rather than actual physical defects are used to identify a location on a designated chromosome.  To find markers, a group of individuals is chosen based on a high incidence of a selected disorder.  Blood samples are then drawn and submitted to a lab.  Researchers proceed by examining different chromosomal markers to determine whether any of them align more consistently with group members who have the disorder or with group members who do not.  If a marker lines up well enough to produce an LOD score of 3 or greater, then the researchers submit the study for publication.  But, once again, all that has been found is a marker with a probability score.

 

With thousands of possible markers and hundreds of researchers looking at thousands of different groups of research subjects all over the world, sooner or later markers will line up just by chance.  This chance alignment is called a "false positive" and results in the retraction of a published study.  Consequently, research journals often incorporate one retraction after another.

 

For example, in 1987 Janice Egeland thought she had found the first marker for a gene for manic depression because she had achieved an LOD score of almost 4.  When another marker was located, the LOD score then approached 5.  At that point and with great professional excitement her study was published.⁴⁵ Subsequent to the date of publication, however, additional data became available which changed the diagnoses of some of the control group members.  This change in diagnoses caused the LOD score to plummet to 2 and her study was retracted

 

The truth is that there are many ways to manipulate the research to raise the LOD scores and there is much debate over this issue in the literature.  LOD scores can be inflated using multiple testing, the use of non parametric tests to analyze the data, shared data, and expanding the diagnostic parameters.^46,47

 

The disappointing results in the area of genetic research has led Kenneth Kendler, M.D., and his associates to state, “Schizophrenia has never yielded up her secrets easily and perhaps some unknown bias—or remarkably back luck—has conspired to produce spurious findings in all these areas.”⁴⁸ Such a statement is equally true for the search for a defective gene in all other areas of mental illness.

 

Now that nearly the whole human genome has been searched and no mental illness genes have been found, researchers are asserting that dozens of genes may be involved in the etiology of any given mental illness.  Furthermore, that they have been unable to locate any of these genes because each contributes just a small portion to the causality.  It appears that this new multi-gene model is just another way of denying defeat, enhancing the myth, and offending the interest of the public and those who fund the research.

 

 

False Pillar #4: The Brain Imaging Pillar

 

Because no actual physiological evidence has ever been found to support the medical model for mental illness, brain scans have become the IV for the ailing medical model.  Two types of brain scans are conducted--structural and functional.

 

Structural studies analyze and compare the anatomy and physical dimensions of the brain.  The goal is to determine whether a diagnosed mental disorder such as schizophrenia is due to a change in the structure of the brain, and the brain is measured to see whether a difference exists between the "schizophrenic" brain and the "normal" brain,

 

In functional studies scientists explore how the brain works when it performs certain tasks.  They accomplish this by recording the way in which the brain metabolizes glucose.  Because glucose (sugar) is brain cell fuel, it serves as a useful substance for identifying which parts of the brain are the most active metabolically.  The goal is to see if those diagnosed as mentally ill process glucose in a different way than do normal people.

 

 Structural Brain Scans:  Below is a set of magnetic resonance imaging (MRI) pictures.  The image on the right is that of a person diagnosed as schizophrenic.  It reflects an enlargement in the lateral ventricular area (notice errors) of the brain.  The brain scan of a non-schizophrenic or normal person on the left shows no enlargement.  Are these images actual biological evidence of mental illness?

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Researchers Chua and McKenna decided to take an honest look at all the brain scan research concerning schizophrenia.  They published a massive 20-page journal article in the British Journal of Psychiatry and reported that the most "consistently replicated brain abnormality is structural, and takes the form of lateral ventricular enlargement."⁴⁹  Even with this finding, they called it a "risk factor" not necessarily connected to the cause of mental illness.

 

Actually this meager evidence on which the biological researchers rely can be explained quite easily from an environmental perspective.  It is true that some ventricular enlargement is found, as well as some atrophy in the hippocampus and cerebral cortex of the schizophrenic brain.  But just because such "evidence" is seen or associated with a disorder such as schizophrenia does not mean that this evidence is the result of a yet-to-be-discovered disease.  Even researcher E. Fuller Torry who is a medical model adherent admits that such differences could be caused by the patients' medications, their diet, and/or environmental stress.⁵⁰

 

Since researchers do not know what causes schizophrenia and they have never seen any physiological evidence of "schizophrenia in action," it is impossible to claim that schizophrenia is responsible for such differences.

 

On the other hand, there is well-established, non-disputable evidence that stress can both enlarge the ventricular areas of the brain as well as destroy neurons in exactly the same areas where atrophy is sometimes found.  Under stress more cortisol is secreted into brain tissue; the brain loses its ability to hold water and shrinks slightly.  This shrinkage of brain tissue bears an inverse relationship to ventricular enlargement.⁵¹  Furthermore, research over the last decade has revealed that the prolonged effects of cortisol secreted from the adrenal gland can result in premature neuronal death in the hippocampus and cerebral cortex.⁵²

 

Thus, once again, researchers claim evidence of a disease purely on hypothetical grounds, but much more evidence exists for an environmental explanation.  Those diagnosed as mentally ill endure a tremendous amount of stress; they worry excessively.  Those who don't worry about how people view them, or who is after them, may worry about the side effects of their medications, where they will live, how they will make financial ends meet, why they are unable to establish friendships, when will the next horrifying hallucination occur, whether anyone will ever love them, etc.

 

In addition to inconsistent brain scan studies and the effects of stress, a final explanation for any purported biological "evidence" is psychiatric treatment itself.  There is a growing body of research that unfortunately indicates that psychiatric drugs cause some form of brain damage (i.e., tardive dyskinesia).  Therefore, some of the atrophy or enlargement which is claimed to be "evidence" may really be due to the "treatments' imposed on the mentally ill by the psychiatric community itself.

 

Finally, at the 1998 state conference for the California Association for the Mentally Ill (CAMI), Dr. Steven Potkin was lecturing to parents on this subject.  As the head of research on schizophrenia at the University of Irvine, he certainly keeps current with the research.  While he was lecturing on this very subject, he was holding up two photographs very similar to the ones above.  He was trying to convince the audience that the differences seen in the photographs were evidence of brain atrophy.  Then, suddenly, he put the picture of the “normal” brain behind his back while still holding the picture of the “mentally ill” brain up in front of everyone.  He then shared that if he took this picture to a radiologist, the radiologist would tell him that there was nothing wrong with the brain.⁵³  In other words, even though some differences are found some of the time in a few patients, these differences are still within the normal range.

 

 

Functional Brain Scans

 

The functional studies are even easier to understand.  To reiterate, functional brain scans measure glucose metabolism.  The brain scans simply pinpoint and measure the most active parts of the brain.

 

When differences in metabolism are found, there is no way to discern whether those differences are the result of some defect or simply are indicative of the brain's response to a stressful situation.  For example, a dog trainer suddenly encountering a stray dog would most likely feel comfortable with the situation, stooping down to greet the dog and offering words of comfort; a person unfamiliar with dogs and previously traumatized by a stray dog, however, would likely panic.  A functional brain scan of the dog trainer and the person experiencing panic or fear would register differences in glucose metabolism.  What would those differences mean--that the person whose brain is working harder with respect to glucose metabolism because he is experiencing fear, has a defective brain? The probable answer is that his brain is working harder because the person is under stress.

 

More specifically concerning schizophrenia, several studies have found a condition known as “hypofrontality,” especially when the individuals studied were performing a neurological task.⁵⁴  Hypofrontality is a condition where less glucose is being processed in the frontal lobes.  So, if so-called schizophrenics process less glucose in the frontal lobes, even though the differences are small, is this proof that schizophrenia is a biological disorder?

 

Many labeled schizophrenics were severely abused as children and/or have suffered a lot of pain enduring the psychiatric system.  When any of us is subjected to a lot of pain, there is a natural tendency to numb ourselves to that pain.

 

For example, prisoners of war often endure tremendous pain and to survive must cut off or deaden themselves to the awareness of that pain.

 

I was taking to a survivor of psychiatric abuse who had first been hospitalized in the 1940s.  She said that the staff would wrap her tightly in ice-cold, wet sheets and leave her wrapped up for hours.  She became very hostile about the treatment but knew if she expressed her anger, her anger would be seen as inappropriate behavior and would lead to more “treatment.” So she trained herself to shut her system down, going into a slight catatonic state.  She was subsequently diagnosed with schizophrenia.

 

When you talk to adults who were beaten as children, they will tell you how they were able to numb themselves to the pain in order to survive the abuse.

 

All of these individuals may show some pattern of hypofrontality or some other way in which they are forced to use their minds differently.  Hypofrontality is not an indication of a disease; it is an indication of the mind’s adjustment to emotional pain.

 

Examining this topic, I interviewed a researcher who specializes in functional brain scan studies and who has access to the most advanced and accurate equipment now available.  I asked him point blank "How do you know whether these image differences are evidence of a defective brain or instead are evidence of the brain's reaction to stress?"  He told me that there is no way of knowing, but the conclusion is that the evidence reveals a defective brain because the identical twin concordance rate for schizophrenia is 50%.

 

This researcher is confessing that he publishes papers in the top scientific and medical journals declaring that he has found evidence of brain damage even though, as he also confesses, he is not really sure what the evidence suggests.  To support his position he must rely upon inaccurate twin study conclusions.  During our discussion, he appeared to be unfamiliar with the equal environmental assumption and quickly ended our interview once I brought up the subject.

 

 

One Hundred Years of Medical Nonsense

 

After over 100 years of branding, bloodletting, spinning, convulsing and drugging the mentally ill based on research using empirical "evidence" together with "evidence" produced through the use of the most expensive and advanced equipment and the latest in drug designs, outcomes have not significantly improved nor has any biological evidence been shown. Scientists have not been able to find one defect, one lesion, one chemical imbalance or one gene that causes mental illness.  All that has been found is hypothetical, based on assumptions that neurobiological defects exist with respect to mental illness and on an untenable and arbitrary labeling of symptoms/behaviors.

 

In 1997 John Horgan, senior writer at Scientific American, accurately summarized the current status of the medical model for mental illness.  With respect to the defective gene pillar, he says that the media has proclaimed the discovery of genes for schizophrenia, manic depression, and alcoholism, but that none of the claims "have held up to the scrutiny of other researchers."⁵⁵

 

He further states that "all this work [regarding brain scans] has failed to yield either a powerful new theory of the mind or truly effective treatments for its assorted disorders."⁵⁶  He indicates that Prozac and other antidepressants are no more effective than talk therapy and then summarizes the current state of psychiatric treatment as follows: "The hot, up-and-coming treatment for severe depression, and even schizophrenia and other intractable disorders, is electroshock therapy, which can cause severe memory loss and other side effects.  Is that a sign of progress?"⁵⁷

 

Colin Ross, M.D., one of the editors of Pseudoscience in Biological Psychiatry published in 1995 concludes that "Biological psychiatry has not made a single discovery of clinical relevance in the past ten years, despite, hundreds of millions of dollars of research funding."⁵⁸

 

Just as the director of the graduate program in psychology was highly influenced by the news article claiming that a gene for schizophrenia had been found, we all can sustain an erroneous imprint by the hoopla and fanfare which accompanies the release of new information regarding the latest twin studies, the latest new drug, the latest marker found, or the latest use of brain imaging technology.  An honest examination of the propaganda (especially the operation of the Four False Pillars) presents a much different picture than that painted by biopsychiatry.  Other branches of the scientific and medical communities have made great strides in the past 100 years, but biopsychiatry has not.  It is obvious that we have all been seduced by one hundred years of medical nonsense.

 

 

References:

 

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2.       Andreasen, N. (1999). Understanding the causes of schizophrenia. The New England Journal of Medicine, 340(8). Pp. 645-647.

3.       Maxmen, J. S., & Ward, N. G. (1995). Essential psychopathology and its treatment. New York: W. W. Norton. P. 57.

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5.       American Psychiatric Association. (1998). Textbook of psychopharmacology. Washington, DC: American Psychiatric Press.

6.       American Psychiatric Association. (1999). Textbook of psychiatry. Washington, DC: American Psychiatric Press.

7.       Andreasen, N. (1984). The broken brain. New York: Harper & Row.

8.       Keffe, R. S., & Harvey, P. D. (1994). Understanding schizophrenia. New York: The Free Press. P. 128.

9.       Koplewicz, H. S. (1996). It’s nobody’s fault. New York: Times.

10.   Comings, D. E. (1996). Search for the tourette syndrome and human behavior genes. Duarte, CA: Hope Press.

11.   Kraepelin, E. (1909-1913). Psychiatrie, 8^th ed. Leipzig: J.A. Barth.

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13.   Tienari, P. (1975). Schizophrenia in Finish male twins. British Journal of Psychiatry Special Publication, No. 10, M. Lader (Ed.). Pp. 29-35.

14.    Torrey, E. (1992). Are we overestimating the genetic contribution to schizophrenia? Schizophrenia Bulletin, 18(1). P.159.

15.   Hoffer, A., & Pollin, W. (1970). Schizophrenia in the NAS-NRC panel of 15,909 veteran twin pairs. Archives of General Psychiatry 23. Pp. 469-477.

16.    Joseph, J. (1998). Rethinking the genetic theory of schizophrenia: A critical review of schizophrenia twin and adoptive studies. Unpublished manuscript, Alameda, CA: California School of Professional Psychology. P.19.

17.   Rosenthal, D. (1970). Genetic theory and abnormal behavior. New York: McGraw-Hill.

18.   Kety, S., Rosenthal, D., Wender, P., and Schulsinger, F. (1968). The types and prevalence of mental illness in the biological and adoptive families of adopted schizophrenics. In D. Rosenthal, & S. Kety (Eds.), The transmission of schizophrenia (pp. 345-362). New York: Pergamon Press.

19.   Rosenthal, D., Wender, P., Kety, S., Schulsinger, F., Welner, J., & Østergarrd, L. (1968). Schizophrenics' offspring reared in adoptive homes. In D. Rosenthal & 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. 15-26). New York: Pergamon Press.

20.   Wender, P., Rosenthal, D., Kety, S., Schulsinger, F., & Welner, P. (1974).                                                                                      Crossfostering: A research strategy for clarifying the role of genetic and experiential   factors in the etiology of schizophrenia. Archives of General Psychiatric, 30. Pp.121-128.

21.   Wender, P. (1977). Archives of General Psychiatry, 34. P. 777.

22.   Rosenthal, D. (1970). Genetic theory and abnormal behavior. New York: McGraw Hill. Pp. 131-132.

23.   Lewontin, R., Rose, S., & Kamin, L. (1984). Not in our genes. New York: Pantheon. P. 227.

24.    Lidz, T. & Blatt, S. (1983). Critique of the Danish-American studies of the biological and adoptive relatives of adoptees who became schizophrenic. American Journal of Psychiatry, 140 (4). Pp. 426-435.

25.    Breggin, P. (1991). Toxic psychiatry. New York: St. Martin’s. P. 98.

26.   Lewontin, R., Rose, S., & Kamin, L. (1984). Not in our genes. New York: Pantheon. P. 223.

27.   Hutchings, B., & Mednick, S. (1975). Registered criminality in the adoptive and biological parents of registered male criminal adoptees. In R. Fieve, D. Rosenthal, & H. Brill (Eds.), Genetic research in psychiatry (pp. 105-116). Baltimore: The Johns Hopkis Press.

28.   Breggin, P. R. (1997). Brain disabling treatments in psychiatry. New York: Springer. P. 5.

29.   American Psychiatric Association. (1998). Textbook of psychopharmacology. Washington, DC: American Psychiatric Press.

30.   American Psychiatric Association. (1999). Textbook of psychiatry. Washington, DC: American Psychiatric Press.

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32.   Breggin, P. R. (1991). Toxic psychiatry. New York: St. Martin's.

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48.   Ibid. P. 126.

49.   Chua, S. E. & McKenna, P. L. (1995). Schizophrenia--a brain disease? British Journal of Psychiatry, Vol. 166. Pp. 563-582.

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52.   Ibid.

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54.   Chua, S. E. & McKenna, P. L. (1995). Schizophrenia--a brain disease? British Journal of Psychiatry, Vol. 166. Pp. 563-582.

55.   Horgan, J. (1997, March 2). Limitless promise, limited delivery. Los Angeles Times. P. M-1.

56.   Ibid.

57.   Ibid.

58.   Ross, C. A. (1995). Errors of logic in biological psychiatry. In Ross, C. A. & Pam, A. Pseudoscience In Biological Psychiatry. New York: John Wiley & Sons, Inc.. P. 116.