The Four False Pillars of Biopsychiatry

Ty C. Colbert, Ph.D.

In order for individuals to fully affirm a non-biological model of

mental illness, it will be necessary to have a solid understanding of the
main fallacies behind the biological model. Even though biopsychiatric
researchers are willing to admit that, to this date, no pathophysiological
or cause-and-effect evidence exists, they still consistently claim that they
are getting closer and that they are making great strides with the new
technology now available to them.
For example, a major textbook on psychiatry, concerning possible
biological evidence for schizophrenia, states,
The past five decades have borne witness to an impressive period of
discovery in the neurobiological basis of schizophrenia. Modern
psychiatric research has produced an abundance of evidence
supporting the notion that schizophrenia is a disorder primarily
related to brain dysfunction.1

Yet, hidden within this quote is the admission that, as yet, nothing
conclusive has been found. In fact, to better affirm that absolutely no
pathophysiological evidence has been found, refer to the National
Institute of Mental Health’s website on schizophrenia.2 Since they fund
much of the research on mental illness, this website will give an instant
update if any true physiological conditions have been found. [I will quote
directly from this website at the end of this paper.]
In reference to the quote from the textbook, the author used the
term “supporting the notion.” The main question then becomes: If I and
so many others in my field claim that no pathophysiological evidence
exists, how did this notion or possible myth come about?
In order to answer this question in a brief manner, as well as
present the material in an easy-to-digest form, I will need to condense
the research considerably. To do so I will address the main biological

Four False Pillars 1

evidence that is most often presented to the public as well as found in
the major textbooks on psychopathology. Thus, after reading this
material, a student or a professional should be able to go to his or her
textbook and identify the major problems with the biological model.

A note before we start. Even though I have attempted to present the

research in as easy-to-understand a manner as possible, such research
may be new to many readers. Because of the importance of this research
in terms of making critical and lifelong decisions for those suffering
emotionally, it is well worth the extra time and effort to properly
understand this material.

The Basic Fallacy

If there is supposedly an “abundance of evidence” to support a biological
model—although I and many other professions still do not believe that
such evidence will ever produce any cause-and-effect results—where
then is the basic problem, and how does such a difference of opinion
exist? Or, if I and others are right, how can so many highly intelligent,
well-meaning, and educated researchers be wrong? In fact, how can the
vast majority of professionals be wrong?
The problem is not so much in the research methodology, but in
the basic assumption that precedes the research. When a person
examines the research data, the data can often point towards either a
biological or environmental conclusion. Thus the conclusions drawn from
the research data are not based primarily on the data, but on the
personal assumptions of the researchers. Figure 1 diagrams this point for
further clarity.

Figure 1. Conclusions based on personal assumptions.

Obviously, the above point regarding researchers’ personal

assumptions is true because, once again, no pathophysiological evidence
has been found and both sides admit to this. So the big question then
becomes, “What assumptions, biological or environmental, are

Four False Pillars 2

incorrect?” One of the main goals of this report is to answer this
question.

The Four False Pillars of Biopsychiatry

To expose the basic fallacies behind the research used to attempt to
establish a biological basis for mental illness, I have divided the research
into what I refer to as The Four False Pillars of Biopsychiatry. These four
pillars are as follows:

False Pillar #1: The Inheritance Pillar: Mental illness runs in families;
therefore, mental illness must be inherited.
False Pillar #2: The Chemical Imbalance Pillar: Medication works by
correcting a chemical imbalance; therefore, mental illness must be
a disease.
False Pillar #3: The Defective Gene Pillar: Defective genes have been
found for some disorders; therefore, mental illness must be a
genetic disorder.
False Pillar #4: The Brain-Imaging Pillar: Evidence of a “diseased”
brain can be detected using modern brain-imaging instruments.

I will now briefly address the main tenets and fallacies of each
pillar. Even though I will not present an exhaustive analysis of the
research, once you understand the basic fallacies to each pillar, you will
be able to understand the fallacies behind the new research or theories
that will most likely be proposed in the future.

False Pillar #1: The Inheritance Pillar

Mental illness runs in families; therefore,
mental illness must be inherited.

How many times have you either heard or read that “since mental illness
runs in families, it must be inherited.” The truth is that an almost
unlimited number of behavioral traits can run in families that are not
genetic, such as language, food preferences, accents, religious and
cultural beliefs, and the way people walk, talk, and so forth.
So how do researchers attempt to prove that mental illness is
inherited? Before I answer this question, let me tell you that this pillar is
perhaps the most important pillar of the four. In fact, as this pillar falls,
so do the rest of the pillars.
This pillar is extremely important because, if researchers can
illustrate or come to believe in some way that mental illness is inherited,
they can then assume that defective genes are involved. Thus, if mental

Four False Pillars 3

illness is inherited and defective genes are involved, then biological
psychiatry can literally (and it has) run into a thousand dead ends but
still continue to believe in a biological model. In other words, if through
studies researchers can conclude that mental illness is inherited, even
though no defective genes, chemical imbalances, or anything else has
been found, researchers can continue to believe in their basic model.
But, if this one pillar is false, then for the most part, the rest of the
pillars collapse.
The inheritance pillar is basically supported by three sources of
data: (a) family statistics, (b) twin studies, and (c) adoptive studies. Once
again for simplicity, I will focus on the research for schizophrenia. But
remember, the argument presented for schizophrenia can be applied to
the other mental health conditions, especially mania, depression, and
ADHD. In fact, researchers Leo and Joseph state,
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.3

Let’s now start our analysis of this pillar with family statistics. But
before we start, I need to state that much of the following information
has come from the excellent investigative work done by Jay Joseph, PhD.

Family Statistics
Figure 2 is a typical graph of the rate of schizophrenia among relatives
that is found in most basic psychology textbooks. The data for this graph
originally came from Irving I. Gottesman’s book, Schizophrenia Genesis.4

Figure 2. Rates of schizophrenia among

relatives of schizophrenia.

Four False Pillars 4

 As you can see by the graph, the closer the genetic relationship,
the greater the concordance rate. According to geneticists, this is
substantial proof that genetics plays a major role in the etiology of
schizophrenia and other mental health disorders.
Even though, according to researchers Joseph and Leo, the data
and methods used to develop this graph are loaded with major
methodological errors,5 the data can still be interpreted one of two ways.
First, the results can be seen as evidence of a genetic component. On the
other hand, such rates could also indicate the importance of the family
environment in the development of schizophrenia. Thus, the only correct
and logical conclusion that can be drawn from this graph is that the
family can play an important role in the development of the symptoms of
schizophrenia as well as other mental health disorders.

Studies of Twins
As shown in the Figure 2 graph on family statistics, the identical-twin
concordance is close to 50% (48%). If you look at any of the textbooks on
psychopathology, the rate quoted will be from 40% to 50% and even
higher. In fact, the National Institute of Mental Health (NIMH) states that
“The identical twin of a person with schizophrenia is most at risk, with a
40 to 65 percent chance of developing the disorder.”6
Of all the data pertaining to the different pillars, this figure is the
most important and most widely used figure to support a genetic model
and thus the biological model in general. For example, a research article
may start off with something like, “Since the concordance rate for
identical twins is about 50%, we can assume that schizophrenia is a
biological disorder.”
As another example, I was attending a seminar where the
presenter was discussing the efficacy of a new antipsychotic drug. The
very first slide in his presentation was a big “50%” that covered
practically the whole screen. The presenter, a psychiatrist from a major
research university, then said, “Since the identical twin concordance rate
for schizophrenia is 50%, we can conclude that psychiatric medication
works by correcting a chemical imbalance due to genetic defects.” With
this assumption, he went on to attempt to sell the benefits of that
particular drug to an audience consisting of fellow psychiatrists.
A twin-studies research project is basically set up in the following
way. To determine the concordance rate between identical twins, first the
researchers locate a group of individuals who have been diagnosed with
schizophrenia and who also have an identical twin. Then the researchers
attempt to locate the other identical twin to determine whether or not
that twin has been diagnosed with schizophrenia. Then a concordance
rate is calculated.
For example, let’s say the researchers located an original group of
100 identical twins diagnosed with schizophrenia (called probands).

Four False Pillars 5

Then, when the twin siblings have been located, let’s assume 47 out of
the 100 have also been diagnosed with schizophrenia. The concordance
rate for this study would then be 47/100 or 47%.
Let’s now take a look at the actual data that is used to support this
40% to 50% and higher figure. Figure 3 lists the published studies
between 1920 and 1987.

Figure 3. Schizophrenic twin studies with corresponding

pairwise MZ concordance rates.7

These are pairwise rates, but some studies also reported proband-
wise rates. Notice that the monozygotic (MZ) rate using the pairwise
statistical method of all the studies is 40%, not 50%. A proband-wise
statistical method was developed specifically for studies conducted
regarding schizophrenia. It, however, inflates the average rate closer to
the 50% often quoted.
Whereas in the pairwise method the probands are counted only
once, they are counted twice in the proband-wise method if each of a pair
of twins concordant for schizophrenia is determined independently.
For example, assume Joan and Joanne are identical twins, both
diagnosed with schizophrenia. If in the process of finding 100 probands
of identical twins to compare with their twin siblings, Joan and Joanne
were both in the original 100 proband group, they would be counted as
only one pair in the pairwise method. They would be counted as two
probands (counted twice) in the proband-wise method. It is this double
counting that inflates the concordance rate in the proband method.
Again, it is important to note at this point that we are not
examining actual biological evidence, but numbers that can be easily
manipulated through the use of different statistical methods. Simply
using the proband-wise method rather than the more conservative
pairwise method can often inflate the concordance rate by 25%.8

Four False Pillars 6

 You may recall it was Mark Twain who stated that “There are three
kinds of lies, lies, damn lies, and statistics.”
Second, and more importantly, notice that the studies range all the
way from a high of 69% to a low of 11%. How can such a wide variation
exist with the simple process of figuring concordance rates?
If you notice, most of the higher rates were also from the earlier or
older studies. There were two major interrelated problems with the
earlier studies: (a) poor research methodology, and (b) strong sociological
biases on the part of the researchers.
The research or methodology inadequacies were the result of the
fact that the studies were often not blind (in which researchers were
personally aware of enough of the particulars to insert a bias), the
diagnostic criteria were inconsistent, and at that time, the zygosity of the
individuals could not be determined by medical means.
For example, if one identical twin had been diagnosed with
schizophrenia and placed in a hospital for several years, then, due to his
emotional condition and the extremely poor conditions of the hospital,
several years later this twin may look quite different from the other twin.
If the twins were identical, but not concordant for schizophrenia, the
researchers could eliminate this pair by claiming that the twins were not
identical. This would benefit their results in favor of a higher
concordance rate by boosting the concordant twins found versus the
non-concordant twins.
In one particular recorded example, researchers were investigating
a set of twins, one of them hospitalized and diagnosed with
schizophrenia and the other one still living at home. By interviewing the
parents and neighbors, to the best of their knowledge, this pair was
identical.
When the researchers actually attempted to interview the at-home
twin to determine if the twin male was suffering from schizophrenia, the
parents told the researchers that their son stayed upstairs most of the
time and did not want to come down to be interviewed.
So, was this twin also suffering from schizophrenia (paranoid of
people), or was he simply afraid that if he came down he may be
hospitalized and labeled like his brother? In other words, his fears may
have been legitimate.
But here is the dilemma that the researchers faced in this
situation, as well as in others. If they did not diagnose him with
schizophrenia, this case would swing the data in favor of a non-biological
explanation. If they diagnosed him with schizophrenia, that would swing
the data in favor of a genetic or biological explanation.
In addition, a major sociological bias was involved. Today
researchers use this grossly exaggerated figure (50%) to continue the
myth of a biological model. But the researchers of the earlier studies
used the data for a terrible and deceptive reason.

Four False Pillars 7

 The earlier, more inaccurate, and inflated rates were used to
support the growing eugenics and Social Darwinism movements,* which
claimed that certain groups of individuals (the physically disabled and
especially the “feeble-minded”) should be prevented from procreating.
Evidence from twin studies purporting genetic inferiority lent credibility
to the passage of sterilization laws applicable to these groups first in the
United States and then in Germany. This “evidence” also fueled Hitler’s
racism and provided additional rationalization for the Holocaust.
In order to illustrate the inherent bias of the twin-study
researchers, it is necessary to identify those prominently engaged in the
research. Francis Galton (1822–1911), a British statistician and cousin
of Charles Darwin, became the father of the eugenics movement. He
originated the idea that twin studies would provide a way to measure
differences associated with either inheritance or environment. Yet it was
Ernest Rüdin (1874–1952) who became the recognized founder of
psychiatric genetics.
Rüdin was an internationally known psychiatrist and eugenicist
who firmly believed that schizophrenia was an inherited disorder. His
Munich research department became the pioneering center for the study
of psychiatric genetics. Rüdin conducted the first family-prevalence study
regarding schizophrenia, the results of which were published in 1916.9
While in high school, Rüdin formed a students’ temperance
association and attracted attention for his uncompromising position on
racial hygiene. In 1901, he received his doctorate and went to work for
Emil Kraepelin. In 1903, at the age of 29, Rüdin formulated his program
for a future “racially pure utopia,” and in 1909 he became the senior
physician at Kraepelin’s Munich hospital. The first twin study regarding
schizophrenia was performed by one of Rüdin’s top associates, Hans
Luxenberger. In fact, the authors of four of the first five twin studies
regarding schizophrenia (Luxenberger, Essen-Moller, Kallmann, and
Slater; see Figure 3) were students at Rüdin’s Institute for Psychiatric
Research in Munich, Germany. The above four researchers trained
several of the other researchers, including Shields, Gottesman, and
Fischer.
When Hitler came to power, Rüdin served on a panel with Heinrich
Himmler. Himmler was chairman of the Task Force of Hereditary Experts.
This task force drew up the German sterilization law of 1933 for
“congenital mental defects,” which included schizophrenia and manic-

                                                                                                                       
*
 Eugenics is the study of, or belief in, the possibility of improving the qualities of the human
species or a human population by such means as discouraging reproduction by persons having
genetic defects or presumed to have inheritable undesirable traits (negative eugenics), or
encouraging reproduction by persons presumed to have inheritable desirable traits (positive
eugenics).
Social Darwinism is a 19th century theory inspired by Darwinism, by which the social order is
accounted as the product of natural selection of those persons best suited to existing living
conditions and in accord with which a position of laissez-faire is advocated.

Four False Pillars 8

depressive psychosis. Seven years later, approximately 70,000 mental
patients had been put to death under the Nazi “euthanasia” program. In
1991, psychiatrist Peter Breggin wrote, “Rüdin embodies the direct link
between psychiatry and Hitler.”10 To say the least, twin studies became
the cornerstone of psychiatric genetics and the growing eugenics and
Social Darwinism movements because they purportedly provided the
evidence necessary to label mental illness as a disease and to “purify the
race” by precluding the mentally ill from procreating.

Most Accurate Studies

Some of the later studies, such as Kringlen, Fischer, and Onstad, used
only hospital records that can also create a sampling bias in favor of
higher concordance rates.11 Only two studies use the more accurate,
register-based data and do not use hospital records.12 Figure 4 shows the
results of these two studies (taken from Figure 3. This 17% figure is a
long ways off from the 40% to 65%.

Figure 4. Schizophrenic twin studies using register-based data.

How Rates Can Be Manipulated

Let me now offer you an example of how rates can be inflated over
time. I admit this is an extreme example, but it illustrates what
researchers can do with data when there is no pathophysiological
evidence to support the data.
Hoffer and Pollin’s 1970 study had the second largest sample of
twins and came close to having the twins diagnosed blindly. The study
resulted in an age-corrected concordance rate of 15.5%.13
In 1972, Allen, Cohen, and Pollin re-analyzed the data and came
up with a new concordance figure of 27%.14 When Mary Boyle looked
more closely at their analysis, she noted that the diagnostic criteria had
been widened and that the authors had evaluated each twin pair
knowing their zygosity status.15
The authors admitted that while reviewing the data, “the reviewer
may have been influenced toward seeing more similarities in MZ pairs
than DZ [dizygotic] pairs.”16 This factor would tend to increase the MZ
concordance rate.
Gottesman and Shields, who are strongly biased towards the
genetic model, took the 27% pairwise figure and recalculated it using the
proband-wise method, coming up with a figure of 43%.17 Expanding the
diagnostic criteria even more, in 1991Gottesman came up with a rate of

Four False Pillars 9

53%.18 So by manipulating the data, researchers increased the
concordance rate from an insignificant 15.5% to an overwhelming 53%.
In summary, it is downright discouraging and frightening to
understand that the same highly distorted data that was used to support
the holocaust is now used to support the medical model.

Monozygotic vs. Dizygotic Twin Studies

Another way of using twin studies is to compare the concordance
rates between identical or monozygotic (MZ) twins with same-sex non-
identical dizygotic (DZ) twins.* Since DZ twins only share 50% of their
genes and MZ twins share 100% of their genes, any major differences
can be assumed to be the possible result of a genetic influence.
For example, if you go back to the chart on family statistics
(Figure 2), you will see that the identical twin concordance rate is 48%,
whereas the non-identical (fraternal) rate is only 17%. So is this evidence
of a genetic influence? Not necessarily.
In order for the MZ-DZ difference to show evidence of a possible
genetic disorder, the Equal Environmental Assumption (EEA) must be
validated. The EEA claims that the environmental influences on fraternal
same-sex twins are basically the same as with identical twins. If fraternal
twins experience the possibility of a greater environmental difference
than identical twins, the differences between the MZ and DZ rates could
be accounted for by environmental factors.
Let’s use an example to make sure the EEA is clearly understood.
Compare one set of identical twins where both of them are attractive and
athletic with a set of fraternal twins where one is attractive and athletic
and the other is not as attractive or athletic. The two identical twins will
likely be treated much more alike than the two fraternal twins. The good-
looking athletic fraternal twin will most likely receive more attention than
the other fraternal twin. On the other hand, the good-looking and athletic
fraternal twin may be subjected to much more pressure to succeed.
Regardless, there is a strong possibility that one twin will be treated
much differently than the other and that the twins will also want to be
seen as different.
This is a simple example, but investigators have often reached the
same conclusion. For example, Harold Carter, a twin researcher, writes,
The assumption that the nurture influences are approximately equal
for fraternal and identical twins… seems untenable to anyone who
has had much contact with twins in their own social environment….
Identical twins obviously like each other better, they obviously have
the same friends more often; they obviously spend more time
                                                                                                                       
*
Identical or monozygotic (MZ) twins originate from the fertilization of the same
ovum, whereas fraternal or dizygotic (DZ) twins originate from the fertilization of two
ova.
 

Four False Pillars 10

 together; and they are obviously treated by their friends, parents,
teachers, and acquaintances as if they were more alike than
fraternal twins are.19

In summary, not only do the modern day textbooks, as well as the

researchers, fudge on the twin concordance rates, they also fail to
address the key issue, which is the Equal Environment Assumption.

Adoption Studies
First of all, it is worth noting that adoptive studies are much more
difficult and expensive to conduct. Thus, if conclusive results could have
been deduced from family and twin statistic studies, adoptive studies
would not have been necessary.
Adoptive studies attempt to eliminate the “environmental” factor by
assuming that, since the children in the study have been removed from
their biological families at an early age, the biological family
environmental element can be excluded from the equation. According to
researchers, adoption studies show an elevated risk for schizophrenia
among the offspring of mothers with schizophrenia.20
This simply means that adoptive children of biological mothers
diagnosed with schizophrenia have a greater chance to be diagnosed with
schizophrenia than adoptive children whose biological mothers were not
diagnosed with schizophrenia. Since the environmental element is
theoretically eliminated by the children’s not living with or being raised
by their biological parents, a genetic component is then assumed to exist.
Even though many methodological problems are involved with
adoption studies, the main factor that undermines a genetic conclusion
is the issue of “selective placement.” It has been shown that adoptees
who were born into highly dysfunctional families have a much greater
chance of being adopted into dysfunctional families. Thus, many of the
adoptive children who eventually were diagnosed with schizophrenia
literally started out in one toxic situation and then were placed in
another toxic situation. Lewontin, Rose and Kamin stated that the
selective placement factor alone “undermines the theoretical separation
of genetic and environment variables claimed for adoptive studies.”21
For example, when the data from the most important adoption
study for schizophrenia (Kety et al., 1968)22 was analyzed, it was
determined that selective placement was a major factor, since 24% of the
index adoptive parents had a history of hospitalized mental illness, but
not one single control parent did.
In other words, selective placement had occurred because the
index children (those diagnosed with schizophrenia), who came from
families with a much higher incidence of mental illness, were then placed
in adoptive homes where 24% of the parents had been hospitalized for a
psychiatric condition. Thus, this data would definitely point towards an

Four False Pillars 11

environmental model—not a genetic one. Lewontin, Rose, and Kamin had
some strong remarks in reference to this study in particular:
The schizophrenic adoptees, who indeed had been born into
shattered and disreputable families, acquired their schizophrenia as
a result of the poor adoptive environments into which they were
placed. The fact that one’s adoptive parent goes into a mental
hospital clearly does not bode well for the psychological health of the
environment in which one is reared.23

As with the twin studies, the propaganda for the adoptive method
has been relentless in favor of a genetic model. For the most part, neither
the public nor the professional community is offered a clear and honest
picture of these studies. Yet, in reference to the above schizophrenic
adoption studies, Gottesman and Shields referred to these studies as
“the straw that broke the environmentalists’ backs.”24

Summary of False Pillar #1

Once again, the only conclusion that can be drawn from this pillar
is that the family plays an important role in the emotional development
of the child. But it is improper to conclude by these studies alone that
such disorders as schizophrenia are genetically based.
As a final note, Loren Mosher, who oversaw much of the earlier
research on schizophrenia at the NIMH when some of the major
inheritance studies were funded, stated that Nazi Germany developed the
best genetic research project possible. They either killed or sterilized a
whole population of individuals diagnosed with schizophrenia. Yet within
one generation, the same incidence of those diagnosed with
schizophrenia returned. If the disorder had been truly genetic, such a
quick return would not have been possible.
With this pillar behind us, I will now attempt to progress through
the other three pillars more rapidly.

False Pillar #2: The Chemical Imbalance Pillar

Medication works by correcting a chemical imbalance;
therefore, mental illness must be a disease.
As with the first pillar, I am sure you have heard the saying that
psychiatric medications work by correcting an imbalance. Again, part of
this false belief is based on the validation of the first pillar; that a true
defect of some kind exists. In fact, psychiatrist and researcher Nancy
Andreasen presents the hope of this model in the following quote:
Scientists will create medications that will correct the abnormal
expression of disease-producing genes. Molecular biology will
someday permit us to perform psychosurgery at the level of the
gene.25

Four False Pillars 12

 The chemical imbalance model has been used by psychiatry and
the drug companies to promote the selling of these drugs, claiming in
essence that these drugs are necessary to correct a defect. Such a model
may have made some sense at the beginning.
Soon after these drugs were introduced, it was discovered that they
work by affecting the flow of certain neurotransmitting chemicals. In
order for a neuron to fire, neurotransmitters are released from the end of
one neuron, flow across a small gap to the next neuron, and then attach
themselves to that neuron. If enough of these neurotransmitting
molecules are able to attach themselves, the next neuron fires and the
particular electrical message continues.
At first, science did not have the technology to test or determine
whether chemical imbalances existed. So the two sides, biological versus
environmental, began to battle it out on this issue. The biological side
claimed a chemical imbalance was involved, whereas the environmental
side claimed just the opposite, that the drugs were similar to alcohol or
street drugs, in that they worked by disabling the brain.
Today, science has the necessary technology to determine whether
or not chemical imbalances exist, but none have been found. It is this
fact that has prompted the present (2014) director of the NIMH, Thomas
Insel, to state that “earlier notions of mental disorders as chemical
imbalances or social constructs are beginning to look antiquated.”26 Also,
William Whirsing, M.D., professor of psychiatry at UCLA, stated to a
room full of psychiatrists that “We have been misleading the public about
the chemical imbalance model for 40 years.”27 Finally, ex-director of the
NIMH, Steve Hyman, upon summarizing over 40 years of research
pertaining to the effects of antipsychotic drugs, reported that the use of
the drugs actually creates, rather than corrects, a biochemical imbalance
within the brain and in fact works similar to drugs of choice or street
drugs.28
If you think about it, the disabling model makes much more sense.
How many individuals use alcohol and/or drugs to block out painful
emotions, to live with intense loneliness, or simply to feel relaxed at an
important social gathering?
No chemical imbalances exist, and that is a fact, not a theory.
Drugs may be useful and needed at times, but they do not support a
disease or defect model of mental illness.

False Pillar #3: The Defective Gene Pillar

Defective genes have been found for some disorders;
therefore, mental illness must be a genetic disorder.
Simply put, researchers have searched the entire human genome,
as well as combed the entire world looking for appropriate multiple-
generational families to study. To date, not one single gene for any so-

Four False Pillars 13

called mental illness has been identified. They find markers or
“possibilities,” but when other researchers attempt to duplicate the
results, they cannot, and the original claims have had to be retracted.
Because no single gene has been found for any mental disorder, to
overcome this problem researchers now believe that they are unable to
find a single gene because several genes are involved, each playing a
small role. As “silly” as this conclusion may seem, researchers still plug
along because of—you guessed it—the first pillar. Quoting from an article
titled “Genetic basis of complex human behavior,” the authors stated, “it
is possible that there are no genes of major effect to be found despite
clear twin and adoptive evidence for genetic influence.”29 “Clear
evidence”! Again, without the first pillar, biopsychiatric research would
not have a leg (pillar) to stand on.
At this point I want to move on to the last pillar, the brain-scan
pillar. Researchers are now using brain-scanning equipment to attempt
to find defective genes, so I will finish up Pillar #3 after explaining the
fallacies of Pillar #4.

False Pillar #4: The Brain-Imaging Pillar

Evidence of a “diseased brain” can be detected
using modern brain-imaging instruments.
Because no chemical imbalance, defective gene, or any other
pathophysiological evidence has been identified, this pillar has become
biopsychiatry’s last great hope. With the brain-scanning equipment now
available, researchers can measure or take a picture of actual differences
in the brain of a person diagnosed with mental illness and then compare
it to a so-called normal person.

Structural Studies

Figure 5 shows a set of magnetic resonance imaging (MRI) pictures

that can be found in almost any basic textbook on psychopathology or
general psychology. The image on the right is that of a person diagnosed
with schizophrenia. It reflects an enlargement in the lateral ventricular
area (notice the arrows in the diagram) of the brain. The brain scan of a
non-schizophrenic or normal person on the left shows no enlargement.
Do these images then represent actual biological evidence of a diseased
brain?
A few years ago, researchers Chua and McKenna decided to take
an extensive look at all the brain-scan research concerning
schizophrenia. They published a massive 20-page journal article in the
British Journal of Psychiatry reporting that the most “consistently
replicated brain abnormality is structural, and takes the form of lateral
ventricular enlargement.”30 Even with this finding, they called it a “risk

Four False Pillars 14

factor,” not necessarily connected to the cause of mental illness. Before
we go any further, let’s make sure we understand the primary role of the
ventricles in the brain.

Figure 5. Lateral ventricular enlargement differences.

The brain is very soft and jelly-like. It must be protected from

shock because of its considerable weight (approximately 1400 g) and its
delicate construction. Outside the skull, a human brain cannot even
support its own weight.
The brain contains a series of interconnecting chambers called
ventricles. The brain is well protected and supported by the
cerebrospinal fluid contained in the ventricles. The brain’s net weight
immersed in this liquid is only 80 g. Shock from a sudden blow or even
mild jarring is cushioned by the cerebrospinal fluid. Without the
protection of this fluid, the brain would bounce back and forth within the
skull, causing considerable damage.
Figure 6 shows a picture of the ventricular system of the brain.

Figure 6. Ventricular system of the human brain.

The largest chambers of the ventricular system are the lateral

ventricles. Because the ventricles show up vividly on imaging
instruments, they serve as important structural landmarks. When parts
of the brain have atrophied (shrunk), the ventricles enlarge to
compensate; therefore, they are important indices of possible brain
diseases.

Four False Pillars 15

 With evidence of a ventricular enlargement in the brain of a person
diagnosed with schizophrenia, and with the assumption that
schizophrenia is a disease, it would only be natural to assume that the
brain had atrophied due to the disease of schizophrenia, whatever that
is. But because no pathophysiological evidence of a disease has been
found, perhaps there are other explanations for ventricular enlargement
(brain atrophy or shrinkage). In fact, stress may be the major factor.
When someone is under stress, more cortisol is secreted into the
brain tissue area than is secreted under normal circumstances. As a
result, the brain loses some of its ability to absorb water. The brain then
shrinks slightly because it is holding less water, not because it is affected
by some disease.
As the brain shrinks, the ventricular areas must become larger,
with more cerebrospinal fluid used to make up for the difference in
volume.
In other words, just as our body perspires or begins to shiver to
compensate for body temperature changes, the ventricular area increases
and decreases as an adjusting mechanism. Thus, the enlargement is not
a pathophysiological state but a natural protective process.
In addition, such factors as depression, early childhood trauma,
and alcoholism can result in ventricular enlargement.31

Loss of Gray Brain Matter

As brain-imaging equipment and technology have advanced, the
claim that schizophrenia and bipolar disorders in particular are true
brain diseases has also increased. The following is an actual set of MRI
brain scans showing how the loss of gray matter (brain cells) has spread
over time.32
To obtain these images, measurements of a group of diagnosed
individuals is compared to a group of non-diagnosed individuals to see if
there is a loss of gray matter over time. As the images are taken, every
two years for example, without a doubt the images do show a loss of gray
matter in the diagnosed individuals versus the non-diagnosed
individuals. In Figure 7, the red (versus the blue) areas illustrate where
the loss has occured.*

Figure 7. Loss of gray matter over time.

                                                                                                                       
* Visit (www.schizophrenia.com/family/disease) for better colored pictures.

Four False Pillars 16

 From the perspective of the biopsychiatrists, these results are quite
spectatular and convincing, leading to headlines such as the following:33
Studies of never-treated patients confirm Schizophrenia is a brain
disease.
People with bipolar disorder-or manic depression suffer from an
accelerated shrinkage of their brain.
UCLA brain researchers using a powerful new technique have
created the first images showing the devastating impact of
schizophrenia on the brain…. The findings show how a dynamic
wave of tissue loss engulfs the brain of schizophrenic patients in
their teen-age years.
Lack of gray matter in brain is linked to Schizophrenia and Bipolar
disorder.
It [schizophrenia] moved across the brain like a forest fire, destroying
more tissue as the disease progresses…. scientists detected gray
matter loss of more than 10 percent….

The above headlines represent statements by some of the best

credentialed researchers in the world, using the most advanced
equipment possible. These statements and images can be quite startling
to those diagnosed with a mental illness, as well as to their loved ones.
So, do researchers now have conclusive, non-debatable evidence that the
disorders of schizophrenia and bipolar disorder are true brain diseases?
Let’s first make sure a couple of points are understood before we attempt
to answer this present challenge.

What Is Gray Brain Matter?

Gray matter is made up of neuronal cell bodies. The gray matter
includes regions of the brain involved in muscle control, sensory
perception such as seeing and hearing, memory, emotions, and speech.
In living tissue, gray matter actually has a gray-brown color, which
comes from capillary blood vessels and neuronal cell bodies.

What Can Cause the Loss of Gray Matter?

Actually, a whole list of factors can possibly cause the loss of gray
matter. Some of these include smoking, lack of sleep, lack of exercise,
such medical conditions as fibromyalgia, and, finally, stress. Since there
is considerable evidence and agreement among professionals that stress
can cause the loss of gray matter, let’s look at this element more closely.

Stress and the Loss of Gray Brain Matter

Bruce McEven, head of neuroendocrinology [should there be an e}
at the Rockefeller University in New York, has reported that rats
subjected to repeated exposure to stress experience shrinkage of the

Four False Pillars 17

neurons in the hippocampus and the prefrontal cortex.34 In addition, an
examination of the brains of soldiers suffering from PTST showed a 5 to
10 percent loss of gray matter volume, indicating neuron damage.35
In fact, as far back as 1996, researcher and professor Sapolsky
used MRI brain scanning equipment to show that stress can shrink the
brain. Quoting Sapolsky from a news release, “The work of several
research groups shows links between long-term stressful life experiences,
long-term exposure to hormones produced during the stress, and
shrinking of the part of the brain involved in some types of memory and
learning.”36
So, let me ask the obvious question: Are mentally ill persons,
especially the chronically ill, exposed to any of the above factors? Are
excessive smoking, lack of sleep, lack of exercise, and especially stress
often a part of their daily lives?
I believe so. If there is a loss of gray matter associated with mental
illness, then it seems foolish to assume that some gene or group of genes
can be responsible. Why is it so hard for researchers to put two and
two—or actually one and one—together? Stress sets off a whole bunch of
chemicals in the brain, including cortisol, which has been called the
“death hormone” by Dr. Nicholas Perricone. In his words,
Large amounts of cortisol are toxic when they circulate in our system
for prolonged periods of time. Our brain cells, or neurons, are
extremely sensitive to the effects of cortisol. When cortisol is
circulating at a high level, it causes the brain cells to die.37

Over time, these chemicals damage the brain cells. This is a proven
fact, not a theory. But this does not mean that the symptoms of
schizophrenia (or other major mental disorders) are the result of a
physically defective brain. This is correlational, not causal evidence.

Psychiatric Medications Causing Brain Atrophy

There has also been an ongoing and quite heated argument
regarding whether the medications given to mentally ill persons result in
brain damage. Because both sides can back up their position with
supposedly “valid” research, I will stay away from this debate at this
time, except to say that it makes common sense to me that these drugs,
which are foreign substances to the brain, would eventually have a
destructive effect on the brain. Again, Steven Hyman, the ex-director of
the NIMH, states that these drugs work in a fashion similar to that of
drugs of choice or street drugs. In addition, psychiatrist Grace Jackson
recently reported a tenfold increase in Alzheimer’s and a 25-year
shortening of a person’s life span due to the use of antipsychotic drugs.38
But here is the main point: Whatever causes differences in the
structure of the brain, it is incorrect to conclude that such differences
are related to or cause mental illness. There is substantial evidence that

Four False Pillars 18

such differences are related to emotional and/or environmental stress.
Actually, neither side disputes this “fact”.

Functional Studies

The aforementioned studies are considered structural studies

because they examine different structural parts of the brain to see if
there are actual physical differences between a so-called normal brain
and the brain of a diagnosed mentally-ill person. The other kind of study
or measurement used today is referred to as a functional study.
Functional studies measure differences in the rate of glucose metabolism
to different parts of the brain. Glucose is a form of sugar and the primary
source of energy for brain cells. Like structural studies, functional
studies also attempt to compare differences between someone diagnosed
with a certain mental illness to someone without such a diagnosis.
But, again, this is correlated evidence, not causal evidence. In
other words, just because two things occur at the same time, it is
improper to conclude that one causes the other or is evidence of a causal
event.
Here is the example I like to use to simplify the major error
involved. At the age of seven, my son was attacked by a large dog and
severely bitten. In fact, if the owner had not retrieved the dog, the results
could have been life-threatening.
Several months later I was walking with my son and his friend
across a field when my son spotted a large dog running loose. He
instantly became quite nervous and moved closer to me for protection,
while his friend did not seem frightened at all. If somehow I could have
measured how each of their brains were metabolizing glucose (energy
consumption), I am sure I would have seen some differences. Because of
my son’s traumatized, near-death experience, obviously he would have
been using parts of his brain differently with the threat of another dog
running loose.
So, does that mean that my son’s anxious or fearful reaction was
the result of some brain defect or that his brain was simply operating in
an understandable survival mode? Yet this is exactly how researchers
attempt to draw their conclusions using functional brain-scanning
equipment.
When I was first trying to make sense of this research, I was able
to obtain an appointment with a top brain-scan researcher at a local
research university. After a short time in his office, I finally asked him
how he could determine whether or not the results pointed towards a
biological or environmental conclusion. He told me that no one could,
but since the concordance rate for schizophrenia is 50%, researchers can
conclude that the results indicate a biological origin. When I began to

Four False Pillars 19

discuss the problems with the 50% figure, he suddenly told me he was
quite busy and that he needed me to leave.
It was obvious to me that he knew something about the major
fallacies behind his research conclusions but did not want to admit to it.

New Model and Attempt to Find

Defective Genes
Some of the technological advancements now available to
researchers have resulted in a new approach to locate possible defective
genes. Instead of combing the human genome directly, researchers now
start with evidence acquired from functional brain scans (Pillar #4), then
attempt to locate defective genes from this data (Pillar #3). If genes could
be found, then this would automatically validate Pillar #1 and
subsequently give hope to developing more precise medications to correct
the chemical imbalances (Pillar #2).
The model for this approach is actually quite easy to understand.
The researchers start by first using functional brain scanning equipment
to locate possible differences in how a diagnosed person, versus a non-
diagnosed person, metabolizes glucose. After locating an area in the
brain where there is a difference, researchers then attempt to locate the
genes that are responsible for the activation of that area of the brain.
Once these genes are located, they then attempt to determine if any of
these genes are defective.
Let me return to the dog-biting incident with my son for clarity.
Let’s assume that my son was showing signs of paranoia over going
outside to play without the protection of a parent. Let’s also assume that
the researchers were unaware or did not take the time to become aware
of the dog-biting incident because they were primarily interested in brain
structural and functional differences.
The researchers then subjected my son to a PET scan while they
had him anticipate going outside. Sure enough, a particular part of his
brain was metabolizing glucose at a much higher rate than a normal
person. How then do researchers attempt to find a possible defective
gene from this data?
Several years ago researchers at the Allen Institute for Brain
Science developed an online interactive atlas of the human brain showing
the activity of the more than 20,000 human genes. With this atlas,
scientists can now determine where, in the brain, genes that encode
specific proteins are active. Using the atlas, researchers can zoom in on
brain structures thought to be altered in mental disorders such as
schizophrenia to find the molecular footprint of these diseases.
Such a map could possibly enable scientists interested in the role
of a particular gene or set of genes in, for example, depression, to bypass
the tedious and expensive laboratory work needed to examine possible

Four False Pillars 20

molecular culprits of the disease, one at a time. Instead researchers
could “theoretically” search the atlas to see where in the brain genes are
active as well as what other genes, active in the same regions, may be
involved.
In other words, since researchers now know what genes affect
what areas of the brain, if the researchers simply assume that the
differences that they see is evidence of a defective brain, then defective
genes must be involved. But again, they must go all the way back to
trust the data in Pillar 1 to claim any validation to their conclusions.
So what are the present results as of 2011 using this new
technique of starting from Pillar #4 or brain scans and then attempting
to identify the specific so-called defective genes? Again, when researchers
first began their hunt for defective genes, they were hoping to find one
main dominant gene responsible for schizophrenia. But when no genes
were found, researchers began to claim that part of the problem may be
that as many as 10 genes were involved, each playing a role. Then the
number grew to 20, still with no actual gene found. Soon after that, the
number of possible genes grew again, to 100.
With this new research approach, scientists are now claiming that
perhaps as many as 900 genes are involved.39 Yet not a single one has
been identified as causing any psychiatric condition. Read Colin Ross’s
response to the possible involvement of so many genes:
Imagine if the protein products of each of these hundreds of genes
were identified. Then imagine that the levels and functions of each of
these proteins could be identified in an individual with a mental
disorder. This would require testing for the intracellular concentration
of hundreds of different proteins. Targeting any one of these gene
products would have to take 25–50 medications to reduce his or her
symptoms by 50%. It is hard to imagine how any person could
tolerate the side effects and drug–drug interactions of 25–50
medications.40

In addition, if several hundred or more genes are involved in

schizophrenia, how many others might result in depression and mania?
And what about schizoaffective disorder, a cross between schizophrenia
and manic-depressive disorder? Are there different genes for each
separate disorder? What about schizophreniform, a milder form of
schizophrenia?

Four False Pillars 21

 Summary of the Four False Pillars
The following summarizes the different pillars.

False Pillar #1, The Inheritance Pillar: Mental illness runs in

families; therefore, mental illness must be inherited.
Inheritance studies make a strong case that families can at times
play a key role. But the studies cannot determine if this role is due to
biological or environmental reasons. On the other hand, both
biopsychiatric and non-biopsychiatric followers admit that,
environmentally, the family does play a key role.

False Pillar #2, The Chemical Imbalance Pillar: Medication works by

correcting a chemical imbalance; therefore, mental illness must be
a disease.
With the latest technology, it is possible to determine if a chemical
imbalance exists; none has been found. On the other hand, it is also an
accepted fact that when psychotropic drugs are used, major changes in
the brain occur. For example, with the use of both the older and newer
antipsychotic medications, upwards of 87% of the dopamine receptors
are blocked.41 Quoting Peter Breggin in reference to the antidepressant
Prozac, “the receptors actually die off or disappear”; and with rats, “Up to
60% of some subtypes of serotonin receptors can disappear.”42
Continuing, Breggin stated,
Prozac once again illustrates the principle that the differences
between therapeutic effects and adverse effects are merely steps
along a continuum from mild to extreme toxicity. Drug-induced
feelings of wellbeing can be understood as an early stage along the
continuum from mild euphoria to mania, sometimes combined with a
generalized dulling or flattening of emotional responsiveness and
social sensitivity.43

In other words, the drug does not correct some imbalance but may
make people feel better (there is a powerful placebo effect with this drug)
because (a) it has a stimulant effect, and (b) it helps to suppress the
person’s emotional pain.
Studies have also shown that the drug Ritalin, used for ADHD,
affects the same areas of the brain as cocaine.44 Thus, the only honest
conclusion is that these drugs produce, rather than correct, an imbalance.

Four False Pillars 22

False Pillar #3, The Defective Gene Pillar: Defective genes have been
found for some disorders; therefore, mental illness must be a
genetic disorder.
Again, with the new technology, researches have now scanned the
entire human genome and have not been able to find one defective gene
for any mental disorder. By believing that as many as 900 different genes
may be involved with schizophrenia alone, biopsychiatry is unable to
admit defeat and continues to request additional research funds to keep
their model alive.

False Pillar #4, The Brain-Imaging Pillar: Evidence of a “diseased”

brain can be detected using modern brain-imaging instruments.
Because no pathophysiological evidence such as lesions exists,
brain scans can only measure differences. There is substantial evidence
that these differences are due to stress, drug therapy, and normal
adjustments to difficult situations (i.e., fear of dogs). There is no evidence
that these differences are due to some biological diseased condition.

Test Time
Let’s now see if you can pass a test on the Four False Pillars of
Biopsychiatry. The following is an explanation of the possible causes of
schizophrenia taken directly from the website of the National Institute of
Mental Health on January 25, 2015.45 As you will see, I have identified
the four false pillars in their attempts to give evidence to a biological
model for schizophrenia. My notes are in brackets. I have deleted some of
the irrelevant material. Refer to their website for a full description and
update. The following is a reprint of the pertinent information from their
website, with my added comments shown in square brackets and italics.
________________________
NIMH—What Causes Schizophrenia?
Experts think schizophrenia is caused by several factors. [Obviously they don’t
know yet.]
Genes and environment. Scientists have long known that schizophrenia runs
in families… [Pillar #1] The risk is highest for an identical twin of a person with
schizophrenia. He or she has a 40 to 65 percent chance of developing the
disorder. [A 40 to 65 percent chance? Remember the twin studies? The higher
figures were developed by Nazi supporters of racial hygiene.]
We inherit our genes from both parents [Pillar #2]. Scientists believe [Believe =
nothing found] several genes are associated with an increased risk of
schizophrenia, but that no gene causes the disease by itself… These genetic
differences involve hundreds of different genes and probably disrupt brain
development. [Hundreds and probably?]

Four False Pillars 23

Other recent studies suggest that schizophrenia may result in part when a
certain gene that is key to making important brain chemicals malfunctions.
[Pillars #2 & #3—no chemical imbalance has been found or they would report it.]
Scientists think interactions between genes and the environment are necessary
for schizophrenia to develop. [They are admitting to an environmental factor but
also admitting to no biological factor at this time.] Many environmental factors
may be involved, such as exposure to viruses or malnutrition before birth,
problems during birth, and other not yet known psychosocial factors. [Obviously
scraping the bottom of the barrel for different theories at this point.]
Different brain chemistry and structure. Scientists think that an imbalance
in the complex, interrelated chemical reactions of the brain involving the
neurotransmitters dopamine and glutamate, and possibly others, play a role in
schizophrenia [Pillar #2 again]. [Can’t find an imbalance in dopamine, for
example, so now think an imbalance between neurotransmitters. But since
hundreds of different neurotransmitters, this ought to keep this basic theoretical
model and the research funds coming and going for a long time.]
Also, in small ways [small ways?] the brains of people with schizophrenia look
different than those of healthy people. [Pillar #4] For example, fluid-filled cavities
at the center of the brain, called ventricles, are larger in some [some?] people
with schizophrenia. The brains of people with the illness also tend to have less
gray matter, and some areas of the brain may have less or more activity. [You
know about these concocted results.]
________________________
You can bring up the same website to uncover the Four False
Pillars for depression and ADHD if you wish. Again, I took this
information from the NIMH website on January 25, 2015, and they will
have the most up-to-date information. Even if you are still leaning
towards a biological model, take into consideration the 200-year history
of recovery through the proper use of psychotherapy and the fact that
about one-third of all those diagnosed with schizophrenia recover with
little or no help. In addition, in third-world countries where psychiatric
care is at a minimum, the recovery rate for those diagnosed with
schizophrenia is almost twice as great as in developing countries where
individuals have access to present-day psychiatric care, including
psychotropic medications.46

Four False Pillars 24

 Keys to Defeating the Four False Pillars of
Psychiatry: A Quick Reference

Pillar #1 Family statistics—can’t determine if environmental or genetic.

Twin studies—do not prove the equal environment
assumption (EEA).
Adoptive studies—selective placement invalidates the studies.
Therefore, can conclude only that “somehow” families may
play an important role.

Pillar #2 No chemical imbalances have been found after extensive

research.

Pillar #3 No defective gene found that “causes” any form of mental

illness after searching the entire human genome for years.

Pillar #4 Brain scan studies:

Structural—stress and psychiatric medications can and do
result in brain atrophy.
Functional—differences found are the person’s individual
adjustment to stressful situations.

Some Final Notes

In doing additional research on the four false pillars, I ran across
an article on the Internet titled, “Another blank on schizophrenia gene.”48
The first line of the article reads, “Scientists have drawn another blank in
their search for a universally applicable genetic explanation for
schizophrenia, strengthening [my emphasis] the case for new
approaches.”
The big question then becomes, if they have been searching for
years and have not found a single gene, how does a multitude of dead
ends justify strengthening additional research and, of course, funds for
that research? A few lines further down they give us the answer:
“Schizophrenia is known to involve genetic factors, since people who have
relatives with the condition are more likely to have it, with 40 to 60%
concordance between identical twins.”
Just as these twin studies were fundamentally important to Nazi
Germany, so are they to today’s researchers as the researchers continue
to justify their position against absolutely no pathological evidence.

Four False Pillars 25

 With the lack of any true cause and effect, pathophysiological
evidence, biologically oriented psychiatry may actually be on the verge of
bankruptcy. A May 6, 2013, article in The New York Times quoted leading
experts pertaining to the present state of their “scientific” approach to
the understanding and treatment of those suffering emotionally. Quoting
from the article,
Decades of spending on neuroscience have taught scientists what
they do not know, undermining some of their most elemental
assumptions… The mechanisms of the field’s most commonly used
drugs—antidepressants like Prozac, and antipsychosis medications
like Zyprexa—have revealed nothing about the causes of those
disorders.
Dr. Insel [past director of the NIMH] is one of a growing number of
scientists who think that the field needs an entirely new paradigm of
understanding mental disorders.48

Just recently (October 2014), Scientific American contained an

article, “Why We Need to Abandon the Disease-Model of Mental Health
Care,” reading, in part, “We should not look to medication to ‘cure’ or
even ‘manage’ non-existent underlying ‘illnesses.’” 49
Elsewhere in the article, the author stated, “We must move away
from the disease model, which assumes that emotional distress is merely
symptomatic of biological illness, and instead embrace a model of mental
health and well-being that recognizes our essential shared humanity.”50
Just the other day I received an email from a friend and colleague
who believes much the same as I do concerning the origin of what we
refer to as mental illness. He wrote:
I went to a lecture by one of these leading neuro-researchers from
U.W. of Madison–neuroimaging, whereby, they have their own MRI,
go to our prisons and scan “known psychopaths.” It is true their
brain looks different, and less neurofibers between 2 regions of the
brain; however, out of a room of... oh, I’d say 200 MD/PhDs/etc...
I was the only one that stood up when he said it was a brain
disorder caused by the shortage of these fibers, and said “I’m sorry,
but could the difference be caused by these guys having horrible
experiences growing up in non-perceived nurturing homes, and thus,
what we are seeing is simply the aftermath of a person not having
learned empathy, compassion, and emotional regulation? Isn’t that
data you are showing just correlational data, and thus, you really
can’t say it causes someone to be a psychopath?” The room went
quiet, but to the lecturer’s credit, he agreed completely, apologized,
then said he sometimes gets ahead of himself and does believe it to
be causal, but has not been able to show that yet. The lecture went
on.

Four False Pillars 26

 Unfortunately, the whole biopsychiatric field of research has gotten
ahead of itself but will not admit to it.
As a result of the lack of true pathophysiological evidence, many
prominent psychiatrists have expressed doubts concerning a biological
position for mental illness. A few years ago, Susan Kemker, M.D., wrote:
The fact that I believed this dogma (that biology is the science of
psychiatry) made Pam’s (1990) critique of biological psychiatry
especially unsettling. When I read his work, I felt that my entire
education as a psychiatrist was subject to question. Some of the
studies being scrutinized were known to me as major contributions to
the field. I was shocked to find not a single “landmark” study
emerging as methodologically sound.51

Colin Ross, M.D., Clinical Associate Professor of Psychiatry at

Southwest Medical Center in Dallas, Texas, from whom I earlier quoted,
also wrote:
When I entered my psychiatric residency, I believed that research
had demonstrated the genetic foundation of schizophrenia and had
shown that schizophrenia is primarily a biomedical brain disease.
This view was almost universally accepted at my medical school,
and I never heard serious criticism of it while in training. It was by a
gradual process that I began to become more and more aware of the
cognitive errors pervading clinical psychiatry—unwittingly
demonstrated to me by my residency supervisors.52

In closing, my main hope in witting this paper is that each reader,

regardless of his or her relationship to the field of mental health, will
search for the truth as these two individuals have done. It is the only
responsible path to take.

Four False Pillars 27

 Notes
1. Maxmen, J. S., & Ward, N. G. (1995). Essential psychopathology and its
treatment. New York: W. W. Norton, p. 57.
2. National Institute of Mental Health. (n.d.). What causes schizophrenia?
Retrieved January, 25, 2015, from http://www.nimh.nih.gov/health
/publications/schizophrenia/what-causes-schizophrenia.shtml
3. Joseph, J., & Leo, J. (2006). Genetic relatedness and the lifetime risk for
being diagnosed with schizophrenia: Gottesman’s 1991 figure 10
reconsidered. The Journal of Mind and Behavior, 1, p. 17.
4. Gottesman, I. (1991). Schizophrenia genesis. New York: Freeman.
5. Joseph, J., & Leo, J. (2006). Genetic relatedness and the lifetime risk for
being diagnosed with schizophrenia: Gottesman’s 1991 figure 10
reconsidered. The Journal of Mind and Behavior, 1.
6. NIMH. (n.d.). What causes schizophrenia? Retrieved October, 25, 2014,
from http://www.nimh.nih.gov/health/publications/schizophrenia/what
-causes-schizophrenia.shtml.
7. Joseph, J. (2010). Genetic research in psychiatry and psychology: A critical
overview. In K. Hood, C. Halpern, G. Greenberg, & R. Lerner (Eds.),
Handbook of Developmental Science, Behavior, and Genetics. Boston:
Blackwell, p. 566.
8. Joseph, J., & Leo, J. (2006). Genetic relatedness and the lifetime risk for
being diagnosed with schizophrenia: Gottesman’s 1991 figure 10
reconsidered. The Journal of Mind and Behavior, 1, p. 17.
9. Weber, M. (1996). Ernest Rüdin, 1874–1952: A German psychiatrist and
geneticist. American Journal of Medical Genetics, 67, pp. 323–331.
10. Breggin, P. (1991). Toxic psychiatry. New York: St. Martin’s Press, p. 102.
11. Joseph, J. (1998). A critical analysis of the genetic theory of schizophrenia.
Doctoral dissertation, California School of Professional Psychology,
Alameda, pp. 23–24.
12. Kringlen, E. (1976). Twins still our best method. Schizophrenia Bulletin, 2,
p. 430.
13. Hoffer, A., & Pollin, W. (1970). Schizophrenia in the NAS-NRC panel of
15,909 veteran twin pairs. Archives of General Psychology 23, pp. 469–477.
14. Allen, M., Cohen, S., & Pollin, W. (1972). Schizophrenia in veteran twins: A
diagnostic review. American Journal of Psychiatry, 128, pp. 939–945.
15. Boyle, M. (1990). Schizophrenia: a scientific delusion? New York: Routledge.
16. Allen, M., Cohen, S., & Pollin, W. (1972). Schizophrenia in veteran twins: A
diagnostic review. American Journal of Psychiatry, 128, p. 944.
17. Gottesman, I., & Shields, J. (1982). Schizophrenia: The epigenetic puzzle.
New York: Cambridge University Press.
18. Gottesman, I. (1991). Schizophrenia genesis. New York: Freeman.
19. Carter, H. D. (1940). Ten years of research on twins: Contributions to the
nature-nurture problem. National Society for the Study of Education
Yearbook, 39, p. 247.

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