Title of Course: The Inherited-Insanity Illusion
CE Credit: 3 Hours
Instruction Level: Intermediate
Author: Frederick W. Nolen, PhD
Abstract:
This course critically evaluates the research alleging the inherited, genetically-determined causes of mental
disorders, behavioral disorders, substance abuse and intelligence. There are serious methodological flaws in
all of this research, including the confounding of nature and nurture, i.e., genetics vs. environment. This
course will discuss the significant symptom overlap among mental disorders and its implications for
assessment, diagnosis, and treatment. Finally, it will propose a synthesis of nature and nurture that will take
both sides into account, resolving many problems of diagnosis and treatment in mental health.
Learning Objectives:
1.
2.
3.
4.
5.
List the basic assumptions of the theories of genetic inheritance and environmental causation
Identify the basic paradigm of the concordance rate studies
List potential environmental explanations for twin similarities
Identify two areas of symptom overlap between PTSD and a bipolar manic episode
Summarize the author’s conclusion about genetic transmission of behaviors like criminality
Posttest:
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(www.pdresources.org). We recommend printing the posttest for use while reading the course materials and
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Please Note:
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The Inherited-Insanity Illusion
“Another area for consideration is illustrated by a case study from my own research…that brought out some
startling similarities for two women who were both Baptists and who both considered volleyball and tennis their
favorite sports. They preferred math and English in school and listed shorthand as their least favorite subject.
Both were studying nursing, and both preferred their vacations in historical places. Perhaps most astonishing these two women were not identical twins and were not related in any way.” (Wyatt, 1993)
Introduction
Author’s Note: This manuscript will use the archaic, outdated, generic term “insanity” to subsume all disorders we now
capture under the psychiatric, psychological, behavioral-disorder umbrella merely to accomplish alliteration. As you will
see, I also discuss other supposedly-inherited behaviors: intelligence, drug addictions and criminality.
The notion of inherited mental illnesses has been with us since the dawn of the study of extreme mental disorders. In
1860, the Belgian psychiatrist Bénédict Morel reported the case of a 13-year-old boy who had formerly been a brilliant
pupil in his school but whom, over a period of time, had lost interest in his studies, had become increasing withdrawn
and had appeared to have forgotten everything the he had learned. Morel thought that the boy’s intellectual, moral and
physical functions had deteriorated as the result of hereditary causes and labeled it “demence precoce” (or dementia
praecox, meaning early insanity). The German psychiatrist Emil Kraepelin later observed that most of these cases do not
develop in childhood but more frequently in late adolescence and adulthood.
The early theoreticians relied largely on armchair philosophy with anecdotal support, since the use of scientific research
in mental disorders was isolated from and lagged behind the advent of systematic research in other areas of psychology.
For example, the first psychological laboratory in Leipzig, Germany, founded in 1879, researched the structures of
consciousness, not mental illness. Although Sigmund Freud began studying and writing about mental illness in that same
era, his findings were based on collections of N of 1 case histories with no formal use of the scientific method. The
zeitgeist of the time seemed to be the acceptance of theory as fact without validation of the facts through the scientific
method. It was not until the advent of the school of Behaviorism in the 1920s that John B. Watson, B.F. Skinner and
others began insisting on rigid empirical research. At about the same time in Russia, Ivan P. Pavlov, the digestive
physiologist and psychologist, was using that same scientific research paradigm independently on behavioral questions.
Unfortunately, the two perspectives (nature and nurture) never seemed to become integrated, and the issue remains
largely dichotomized to the current time.
Nature vs. Nurture
Developing a meaningful diagnosis is the starting point to the entire endeavor of all health-care, both physical and
mental. Many of the objections against diagnosing have their limited validity, but most can be eliminated for a variety of
reasons. However, two vigorously opposed orientations regarding etiology have serious consequences regarding the
understanding and treatment of mental and behavioral disorders. Anyone who has taken a high school general
psychology class knows about those two orientations: biological vs. sociological (nature vs. nurture).
An important resolution needs to occur within this nature-nurture conflict if we are to achieve greater meaning and
utility in clinical diagnosis, especially given the broad overlap of categories. The DSM-IV-TR (APA, 2000) warns that
“there is no assumption that each category of mental disorder is a completely discrete entity with absolute boundaries
dividing it from other mental disorders or from no mental disorder.” It also states that “a categorical approach to
classification works best when all members of a diagnostic class are homogeneous, when there are clear boundaries
between classes, and when the different classes are mutually exclusive (DSM-IV-TR, p. xxxi).”
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When it comes to the clash of opposites, the truth is usually some combination of those original polar opposites. This
writer believes that diagnosing can be most effectively conducted by using the biopsychosocial approach (Engle, 1977)
to diagnosis with regard to the contributions of genetic and environmental factors in mental disorders. The
biopsychosocial approach takes into account all aspects of biology, sociology, and childhood experiences, along with
their effects on the current psychological state of the individual. There are, however, some specific issues regarding the
contributions of nature and nurture that are critical for valid diagnosis and effective treatment, which many
diagnosticians do not take into account as they relate to diagnosis and treatment. Those issues include the following:
Correlation Does Not Equal Causation
The figures cited for any concordance (shared familial incidence of severe mental illness) of a mental disorder between
two different people are simple correlation or percentage numbers. As statistics show, neither concordance nor
correlation nor shared-percentages actually equals causation. A classic example given in general psychology class is:
there is a significant positive correlation between the number of telephone poles in a town and the number of bars in
that town. Does that correlation mean that telephone poles cause bars, or that bars cause telephone poles? No. They
are, of course, due to an underlying variable related to both: the number of people in that town.
Genetic Concordance is related to Environmental Concordance
Concordance rate studies for mental illness were initially done by
psychiatrists starting in the 1940s. They used the assumption of genetic
causation that continues into more recent studies using the same
method. For the most part, they all found that identical (monozygotic)
twins had the highest likelihood of shared mental illness. Non-identical
(dizygotic) twins had a lower rate of shared mental illness but still higher
than other family members. Lastly, non-genetically related people had
the lowest coincidence of similar mental illness. The same data patterns
have been reported for shared incidence of mental retardation and
alcoholism (see below). However, none of these studies accounted for
the possibility that genetically similar individuals might also exist in very
similar environments. Later studies that did factor in this interaction –
or at least took environmental effects into account – always showed that the similarity of environments, not the
similarity of genetics, was the most potent explanatory factor for most mental or behavioral problems. Comprehensive
reviews like Jay Joseph’s 2004 book, The Gene Illusion, showed that those early medical studies never took
environmental factors of any kind into their diagnoses.
Post-Traumatic Stress Disorder (PTSD)
PTSD was a new addition to the DSM in 1980. While the psychiatric diagnosticians of the 1940s, 1950s and 1960s were
examining emotional lability and social dysfunction, none of them considered PTSD or its environmental causes as an
etiology or diagnosis for any of their patients because PTSD was not yet included as a DSM diagnosis. Before that,
combat trauma (“shell shock,” “battle fatigue,” etc.) was the only trauma-based category in the DSMs, and it was
considered to be a transient effect of war that usually resolved itself after soldiers returned from combat.
Similarly, many clinicians did not believe their patients’ accounts of sexual abuse, at least partially because of Freud’s
assertion that it was all wishful fantasy. Prior to 1975, there were not even any laws in the United States protecting
children from abuse or neglect of any kind. Physical abuse was just considered a way of punishment following the “spare
the rod; spoil the child” belief system. Of the 15 classic studies listed by Joseph (2004) finding a genetic source for
mental disorders, none mentioned doing a differential diagnosis of PTSD or examining the effects of any abuse. It is
likely that those cases and any others diagnosed without consideration of PTSD or other trauma missed the impact of
environmental experiences on situational and/or chronic mental conditions.
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Symptom Overlap
What are the consequences of the overlap of symptoms of various mental or behavioral disorders? Can that overlap
lead to conflicting diagnoses? Let us take a look by examining the diagnostic subsections of Post-Traumatic Stress
Disorder and see how they overlap with other diagnostic categories. The DSM-IV-TR’s full criteria for diagnosing PTSD in
adults and children are the following:
POST-TRAUMATIC STRESS DISORDER DIAGNOSTIC CRITERIA
A. The person has been exposed to a traumatic event in which both of the following were present:
•
•
The person experienced, witnessed, or was confronted with an event or events that involved actual or
threatened death or serious injury, or a threat to the physical integrity or self or others.
The person’s response involved intense fear, helplessness, or horror. Note: in children, this may be expressed
instead by disorganized or agitated behavior.
B. The traumatic event is persistently re-experienced in one (or more) of the following ways:
•
•
•
•
•
Recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note:
in young children, repetitive play may occur in which themes or aspects of the trauma are expressed.
Recurrent distressing dreams of the event. Note: in children, there may be frightening dreams without
recognizable content.
Acting or feeling as if the traumatic event was recurring (includes a sense of reliving the experience, illusions,
hallucinations, and dissociative flashback episodes, including those that occur upon awakening or when
intoxicated). Note: in young children, trauma-specific reenactment may occur.
Intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of
the traumatic event.
Physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the
traumatic event.
C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present
before the trauma), as indicated by three (or more) of the following:
•
•
•
•
•
•
Efforts to avoid thoughts, feelings, or conversations associated with the trauma
Efforts to avoid activities, places, or people that arouse recollections of the trauma
Inability to recall an important aspect of the trauma
Markedly diminished interest or participation in significant activities
Feelings of detachment or estrangement from others
Restricted range of affect (e.g., unable to have loving feelings) sense of a foreshortened future (e.g., does not
expect to have a career, marriage, children, or a normal life span)
D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the
following:
•
•
•
•
•
Difficulty falling or staying asleep
Irritability or outbursts of anger
Difficulty concentrating (Author’s note: a part of attention deficit disorder)
Hypervigilance (Author’s note: linked to attention deficiency)
Exaggerated startle response (Author’s note: causes attention deficits)
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All of the items noted are the overlapping symptoms of ADD/ADHD and childhood PTSD. In other words, PTSD in
children can easily be mistaken for ADHD due to this symptom overlap.
Note A, 2: In children, this intense fear, horror and helplessness may be expressed instead by disorganized or agitated
behavior. The child and adolescent with PTSD are unable to focus on school or other external tasks because they are
focused on their task: avoiding more abuse. They seem agitated; they are really in chronic “fight or flight” mode.
Note B, 1: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed. They act
out those abuses both in play and in conflicts. Abused children have a higher risk of becoming abusive adolescents and
adults than non-abused children (Main & George, 1985; Pincus, 2001).
Note B, 2: In children, there may be frightening dreams without recognizable content. Even if the nightmare dream
content is recognizable, many healthcare providers who do not understand the manifestations of trauma might assume
that it is just a stage and that they will grow out of it.
Note B, 3: In young children, trauma-specific reenactment may occur. Abused children and adults are more aggressive
with their peers. It is a conflict-resolution method that is learned through modeling (Bandura, 1965).
Note D, 3: Difficulty concentrating is the sine qua non of ADHD and a major defense mechanism of PTSD. PTSD victims
are constantly having recurrent and intrusive distressing recollections of the event(s) (Criteria B, 1), so they are not
totally attentive to here-and-now events. While the non-abused child can be totally focused on class work, class
discussions or class projects, the abused child may be remembering the abuse that happened that morning, thinking
about what new abuses might happen that evening, or planning how to cope with the abuser after school.
Note D, 4: Hypervigilance: while non-abused children or adolescents
are focusing on the project or the discussion, abused children or
adolescents are constantly and unconsciously scanning the current
environment for possible new threats. They look up from their book at
every sound that might be similar to the sounds they heard as they or
other family members were being abused.
While that lapse in considering the potency of trauma may seem
merely academic, it is not. One can also see some of the symptom
overlap between PTSD and other adolescent and adult diagnoses.
Further elaborations on adolescent and adult diagnoses will be
discussed in greater detail later.
People who are physically or sexually abused constitute a high percentage of people who seek outpatient treatment.
Lombardo and Pohl (1997) found that 71% of people seeking outpatient treatment reported being physically abused,
and 38% reported being sexually abused. Sexual and physical abuse is a feature in the majority of those admitted for
inpatient services. People whose parents physically or sexually abused them are very emotional and have some
symptoms that fall into the broad Schizophrenic Spectrum Disorder (SSD) category that was used in many of the earliest
schizophrenia concordance studies.
None of the genetic transmission studies reviewed by this author mentioned that they determined whether the patient
or his/her parents had been brutalized by another person. Reality can be very brutal. Only those clinicians who ask
about brutalities are told about them. Any child who is beaten so badly by an adult that he defecates in his pants has a
high probability of serious lifelong behavioral and emotional problems in all areas of life. A combat veteran who is
captured and tortured is likely to have life-long problems that can include being overly emotional, having social
problems, substance abuse issues, academic problems, occupational challenges, and relationship difficulties. To make
matters worse, as we know, abused children often become brutalizers of both children and other adults (Briggs, 1995).
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While the DSM-IV-TR states that prevalence of schizophrenia is between 0.5% and 1.5%, (p. 308) the estimated
prevalence of sexually abused people in America averages about 25% for females before they reach 18 and 18% in males
(Finklehor, 1984). Many are sexually brutalized, and many more are physically abused. These percentages do not include
the figures for all males sexually abused by priests (over 10,000 by the Catholic Church’s own count in America; 15,000
in Ireland [Allen, 2010]). Nor do they account for the children who are abused by teachers or other adults in positions of
authority in schools, estimated by Shakeshaft (2003) to be 4.5 million students in public schools grades K-12.
While all abuse does not create PTSD, all brutality has a distorting effect on normal emotionality and typical
socialization. In some cases, abuse is not fully assessed by mental health professionals if they are accustomed to making
their diagnosis through the filter of assumed inherited, biochemical imbalance disorders. Therefore, it is possible that
many studies have severely overestimated schizophrenia, dealing in many cases with emotional lability and social
dysfunction that is produced by blatant environmental trauma. See Combat Trauma (Nolen, 2007) for more detailed
elaboration of its manifestations in post-combat veterans and any of the myriad books or scientific research about the
effects of civilian traumatization (e.g., Maltz, 2001; Bass and Davis, 2008).
The intention here is not to minimize other theories about the etiology and treatment of mental and behavioral
dysfunction. Most approaches have their validity and usefulness. However, it is also likely that many diagnosticians stay
within their limited scope of perspective and give labels from their biological or psychological or sociological perspective.
The reality of the patient is that he or she is a biopsychosocial entity and needs to be honored as such. They all have
minds and bodies. All of those facets need assessment in every case.
There are voluminous data showing that the mind and body interact. We know that the
physical state of the body affects the emotional state of the person. Changes in blood
chemistry like variations in potassium, magnesium and sodium levels have an effect on mood
and cognition (Torres, et al., 2008). Chemical changes related to the effects of hormonal
fluctuations during the menstrual cycle affect mood and cognition (Golub & Harrington, 1990;
Golub, 1976). We know that hypogonadism, with its suppression of testosterone, affects male
mood (Matsui, et al., 2009). Conversely, both cognitively pleasing events (getting married, etc.)
and cognitively distressing events (getting divorced, etc.) create massive emotions as well as chemical changes in the
physical body systems. It is not mind or body; it is mind and body. However, it is not a closed-loop debate. It is possible
to differentiate genetic causes from environmental causes in many emotional disorders. It is a crucial differentiation,
which is needed to ascertain the most potent factors for treatment of any behavioral or emotional disorder.
Later in this course we will detail many factors that reduce the reported strength of the genetic relationship of one
family member’s diagnosis to another family member’s diagnosis in the methodologically-poor but extremely influential
early research in this area. These include lack of double-blind rating (the rater for one person is the rater for the other
person); archaic data that diagnosed without any consideration of environmental factors; creation of new, non-clinical
categories of schizophrenia (the Schizophrenic Spectrum Disorder), and many others. The reader is referred to The Gene
Illusion by Jay Joseph or essays such as “The Fallacy of the 50% Concordance Rate for Schizophrenia in Identical Twins”
(Leo, 2003) for particulars above and beyond the many mentioned here.
With the Diathesis-Stress Hypothesis, Rosenthal (1963) tried to strengthen the genetic perspective of schizophrenia’s
cause by saying that “what is inherited is a constitutional predisposition to schizophrenia” (p. 507). He postulated that
people inherit a predisposition that will develop into schizophrenia in the presence of the necessary environmental
triggers (stress). Schizophrenia wasn’t the only arena to postulate this diathesis (split). A non-exhaustive list of studies
on the diathesis concept include PTSD (Elwood, et al., 2009) depression (Nemade et al. 2007), procrastination (Walsh
and Ugumba-Agwunobi, 2002), bulimia (Strober et al., 2000), suicidal attempts (Brezo et al., 2010), seasonal affective
disorder (Provincio, 2008), and helplessness (Boggiano, 1998). Since there has not been any valid, independently
established proof of inheritance of these disorders in the first place, the concept of diathesis is an attempt to elaborate
on the expression of an inherited mental disability without valid data to support the original hypothesis that it is
inherited.
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There have been many scientifically published findings that reportedly identify the inherited aspects of almost all
behavioral and emotional problems of life such as anger (Plomin et al., 1988), sexual orientation (Bailey and Pillard,
1991), intelligence (Bouchard and McGue, 1981; Pedersen et al., 1985), temperament (Plomin and McGuffin, 2003),
alcohol and drug addiction (Rosenthal, 1971; Manzardo and Penick, 2006; Ramoz, Schumann & Gorwood, 2006, etc.),
depression (Moore and Jefferson, 2006), attention deficit-hyperactive disorder (Asherton, Kuntsi and Taylor, 2005),
eating disorders (Kaye, et al., 2008), criminal behaviors (Skeem et al., 2007) and to start it all off, schizophrenia.
Early Schizophrenia Concordance Research
The classic report alleging genetic inheritance of schizophrenia was done by Kallmann (1958, cited in J.C. Coleman,
Abnormal Psychology and Modern Life, 3rd edition, Scott, Foresman and Company, 1964.) His paradigm seems to have
established the template for the research seeking genetic causes for all such conditions. The same paradigm has also
been used to suggest that positive traits like intelligence and personality are also primarily inherited traits.
The table below shows Kallmann’s data, which he used to conclude that schizophrenia was genetically inherited. The
methodological and philosophical flaws in his and other studies purporting to prove that the disorders are genetically
based will be discussed, as well as the environmental factors that can be shown to influence the behaviors more
predictably than any genetic factors.
Table 1: Kallmann’s findings on concordance of schizophrenia as summarized by Coleman (1964, page 286) as:
Relationship to Schizophrenic Individual
Identical Twins
Fraternal Twins
Siblings
Half Siblings
Children (both parents schizophrenic)
Children (one parent schizophrenic)
Unrelated Persons
Percent of Incidence of Schizophrenia
86.2
14.5
14.2
7.1
68.0
16.4
0.85
This layout descending from genetically identical twins to genetically unrelated humans is the standard grid for all of
these studies claiming genetic causation or predisposition for any of these conditions. As genetic similarity decreases, so
decreases behavior similarity. As genetic similarity increases, so increases behavioral similarity. However, careful
analyses of these studies that have reported the same conclusion over decades of time reveal serious flaws. Even though
they have used numerous and varied subject pools, countries of origin and different topics (schizophrenia, depression,
alcoholism, etc.), all share many shortcomings. J. Joseph (2004) outlines a good comprehensive dissection of several of
these areas.
The concordance studies do not prove by themselves that mental illnesses are inherited. The original research done on
this nature vs. nurture conflict was done in a wave of emotion in the 1920s under the topic of eugenics. Eugenics
focused on selective breeding and elimination of tainted or bad blood. Sir Francis Galton, the English-born researcher of
physiology and psychology, coined the word eugenics meaning literally “well-born.” He was also the developer of twin
studies. He wrote, “It would be quite practical to produce a highly-gifted race of men by judicious marriages during
several consecutive generations” (Galton, 1881).
Galton also wrote, “I have collected numerous instances where children of low race have been separated at an early age
from their parents, and reared as part of a settler’s family, quite apart from their own people. Yet after years of civilized
ways, in some fit of passion or under some craving, like that of a bird about to emigrate, they have abandoned their
home, flung away their dress, and sought their countrymen in the bush, among whom they have subsequently been
found living in contented barbarism, without a vestige of their gentle nature (Galton, 1995).”
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In other words, no matter how good their later environment, they are doomed to revert to their savage roots during a
“fit of passion.”
Other experts of those eras wrote things such as the following:
“My own observations, which have been practically unlimited along lines of information connected with the male
offender, have led me to believe, in the last few years, that criminal character depends in the first instance on
heredity…So to the born criminal is the product, mind and body, of the forces of heredity. Not only his body, but
also his mind, is deeply impressed with the character of the parentage. And few indeed are the criminals who
come to our prison at Sing Sing with minds that were at birth a tabula rasa, whose mental powers at birth were
not already thickly sown with seeds of crime.” (Irvine, 1903)
Mr. Irvine’s entire observations were not, in fact, “practically unlimited.” They were limited to watching inmates at Sing
Sing Prison, where he was the warden.
Others even wrote of the inheritance of base, criminal behaviors as inherited by some humans from our animal
ancestry:
“The acts of taking and keeping loose articles, of tearing away obstructions to get at something desired, of
picking valuables out of holes and pockets, of assaulting a neighbor who has something desirable or who has
caused pain or who is in the way, of deserting a family and other relatives, of promiscuous sexual relations-these
are crimes for the twentieth century citizen but they are the normal acts of our remote, ape-like ancestor...
Imbecility and “criminalistic” tendency can be traced back to the darkness or remote generations in a way that
forces us to conclude that these traits have come to us directly from our animal ancestry and have been got rid
of…If we are to build up in America a society worthy of the species man then we must take such steps as will
prevent the increase or even the perpetuation of animalistic strains.” (Davenport, 1911)
These writers were not the propagandists of Nazi Germany. They were European and American scientists of the day,
doing the social science-of-the-day, mostly armchair philosophy. Countries
across the world including Scandinavian countries and Germany developed
eugenics departments and even engaged in sterilization of the tainted
(their word) years before Nazi Germany. However, even though we may
have moved past the post-World War II, hate-everything-about-the Nazis
era (including eugenics), there have still been many researchers trying to
find genetic, biological causes of varied behavioral, psychological and
psychiatric disorders. Most of them seem biased from the start toward the
assumption of a biological determinant. Therefore, their beliefs distorted
their data collection and produced results supporting their initial bias.
A book published in 1881 titled The Science of Life: or, Self-Preservation
had an illustration in it that perfectly illustrated the pre-Nazi racial
prejudices and stereotypes of that day. The illustration shown here is
copied from the book. This is a drawing depicting an English middle-class
family. However, note that the little English boy is dressed in the slippers
and headband of an Indian. This is to designate the boy as retarded, the
publisher believing all readers would understand the implication of the
boy’s attire. The belief of that day was that all Indians were retarded. (The
book is a treatise on the ills of masturbation. The author claimed the little
boy’s parents are gaunt and pale because they masturbated. The author
further claimed their little boy is retarded because the parents
masturbated.)
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Even Kallmann initially wrote in the forward to his 1938 book, “The present study of the genetic and reproductive
conditions in schizophrenia families was undertaken in 1929 in collaboration with the German Research Institute for
Psychiatry in Munich (Prof. Dr. Ruden)…The principal aim of our investigation was to offer conclusive proof of the
inheritance of schizophrenia…” (p. xiv).
Even with non-eugenics proponents, the methods were flawed in serious ways. For example, the first prototypical study
was done by Franz Kallmann. He did the diagnosing on all twin pairs in Table 1, above. He diagnosed first one twin; then
he interviewed and diagnosed the other twin. He knew what the first twin’s diagnosis was before he interviewed and
diagnosed the other. He knew whether a twin was monozygotic or dizygotic. Not surprisingly, his results showed a
genetic link in schizophrenia. Unfortunately, that method bias was the prototype of many influential scientific studies for
the next 70 years. None of their studies used any method to eliminate for experimenter bias.
“Twins Reared Apart” Studies
In addition to the classic studies of Kallmann on twins and other siblings reared together, many researchers (e.g., Muller,
1925; Newman, Freeman & Holzinger, 1937) also assessed twins supposedly reared apart to see if the effect of separate
environments would mitigate the effects of genetic similarity on various measures. However, as Joseph (2004) points
out:
This label is quite misleading because few of the pairs were actually reared apart without knowledge of and contact with
each other.
Twin pairs sometimes were separated only after
having been reared together for several years. Those
years were the early, formative years in which all
they knew was learned unconsciously via modeling.
Pairs were often raised by different members of the
same family. If a twin is raised by an uncle, aunt or
grandmother, there are likely to be similarities to
the child’s parents in socioeconomic status, childrearing methods, disciplinary methods, attitudes
about religion, morality and work.
Pairs were usually placed into families correlated for
socioeconomic status. This was done sometimes by
default since families of the lower and middle classes were more likely to lose and/or adopt children.
Most of the pairs were brought to the attention of researchers due to their similarity and knowledge of each other’s
existence. (Author’s note: some monozygotic twins do not look alike because of in utero catastrophes).
The material used to evaluate both of the twins was collected by the same researcher (non-blind condition, again).
Personality and environmental resemblance was assessed by non-blinded raters.
Some researchers excluded several pairs that showed marked behaviors differences. For example, Newman et al. (1937)
excluded pairs if they answered (“no”) to the following question: “Do you yourselves believe that you are far more alike
than any pair of brothers or sisters you know of?”
Age of separation and the effects of separation were not considered in any of the major studies.
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Regardless of some studies that seemed to support the argument of genetics over environment, the factors listed above
thoroughly weaken the findings in this entire subsection of twin research, along with any of their conclusions regarding
nature vs. nurture.
What definition of schizophrenia did the early researchers use? These studies investigating genetic causes of mental
illness started out with Kallmann’s 1938 heredity study, prior to the publication of any Diagnostic and Statistical Manual.
That was before any standardized, operational diagnostic system was available. So, what were these old-time, pre-DSM
researchers’ criteria for diagnosing schizophrenia? According to Sullivan and Kendler (2003), they were “unstated” for
the classic studies of Essen-Moller (1941), Inouye (1961), Kallmann (1946), Rosanoff et al. (1934), Slater (1953), and
Tienari (1963). Their data and conclusions were accepted because they were either “highly respected researchers,” used
“accepted research practices of their era,” or because of “tradition.” None of the studies employed the scientific
practice of establishing an operational definition.
Schizophrenia is neither a unitary process nor a monolithic
unit. The DSM-IV-TR currently lists five separate subtypes:
Paranoid, Disorganized, Catatonic, Undifferentiated, and
Residual. It used to call Disorganized types “Hebephrenics.”
Some of them (Paranoids and Catatonics) have spectacular and
flamboyantly “hard,” “positive” behaviors (i.e., hallucinations,
delusions, postures). The others (Undifferentiated and
Residual) are more noted for “soft,” absent, “negative”
behaviors (lack of motivation, lack of independence). The
Hebephrenics were just inappropriately silly. “Hebe” means
laughter in Latin. In diagnostic tapes by a psychiatrist named
George Kisker from the 1950s, a woman with nervous laughter
got a diagnosis of hebephrenia.
After decades of effort by DSM committees to narrow and specify disorders, we currently find studies that use more
unified, specified diagnostic criteria from the DSMs. However, one can note that the initial studies of twin-inheritance
eventually widened the criteria for schizophrenia to suit their statistical needs. They developed what they called
Schizophrenic Spectrum Disorders (SSDs). This began with the team of a Danish psychiatrist, Kety et al. (1968). The team
found a small sample (N=16) of chronic schizophrenics (whom they labeled “B1”) and concluded that the sample size
was insufficient to conduct their study. Kety wrote the N of 16 “is too small to give the heritability of such disorders the
proper opportunity to express itself” (in Rosenthal, 1972, p. 68). Therefore, he decided to add what he called “doubtful
schizophrenics: reactive, schizoaffective, borderline or psychoneurotic schizophrenics, or schizoid or paranoid, uncertain
Chronic Schizophrenia, and Inadequate Personality” (Rosenthal, 1971, p. 194.)
Others included people in this SSD spectrum if they were homosexuals, latent schizophrenics, manic-depressives or
“perverts” (Rosenthal’s term). The categories of schizophrenia-like, pseudo-neurotic schizophrenics or latent
schizophrenics do not appear in the DSM-III, or the later DSMs. They also do not appear in the current versions because
they were too vague or imprecise to be meaningful categories when subjected to closer examination by later DSM
workgroups.
Instead of staying within the general spirit of the time calling for increased specificity of definitions in scientific research,
the researchers in genetic heritability of undesirable traits broadened the scope of the definition of schizophrenia to
include just about anyone with problems.
So, when one returns to the more precisely identified people with bizarre, spectacular versions of schizophrenia, one is
left with those who manifest the hard or positive signs of schizophrenia, defined in the DSM-IV-TR, those with
“distortions in thought content (delusions), perception (hallucinations), language and thought process (disorganized
speech), and self-monitoring of behavior (grossly disorganized or catatonic behavior)” (DSM-IV-TR, p. 299).
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Can it even be automatically assumed anyone who has any of these “hard” symptoms is automatically a schizophrenic?
Not automatically, because of the significant symptom overlap between schizophrenia and other syndromes. For
example, dissociative identity disorder (aka multiple personality disorder) also includes the very schizophrenic-like
symptoms of auditory hallucinations. How can one differentiate the schizophrenic auditory hallucinations from DID
auditory hallucinations? The dynamics differ significantly. While both groups’ hallucinations are negative in their impact
on the individual, the true schizophrenic’s hallucinations are flat, repetitious and non-interactive. The auditory
hallucinations scold or berate the schizophrenic patient, and the patient mechanically responds back. By way of contrast,
the DID’s voices are complexly interactive, conversational and have complex consequences. The DID’s auditory
hallucinations are both positive and negative. The DID’s voices have names, faces and separate personalities with
separate memories, emotions and talents. The DID dissociates in space and time, while the schizophrenic does not.
The other significant consideration in making a differential diagnosis of schizophrenia vs. DID is etiology. While
schizophrenia allegedly occurs in a genetically-inherited vacuum, DID patients report 90-95% of the time that they have
been severely sexually abused by many different people starting early in their childhood (Putnam et al., 1986). This is
evidence of environmental causation, not simply of a broken brain or inherited biochemical imbalances.
Confounded Results
Earlier studies accounted for first-degree and second-degree relatives with the same weighting. While seeking to
provide proof of the strength of genetics, the researchers collapsed first and second degree relatives’ ratings of mental
illness in the same category without calculating percentages of influence based on percentage of genetic similarities. If
one wants to accurately assess the influence or impact genetics has on a behavior or trait, one would conserve the
integrity and specificity of the data by coding how much genetic similarity there is between group members. None of
them did that.
Some studies used a five-minute doorstep conversation to obtain their information about the person’s mental status.
People who are severely mentally ill are not known to be overly sociable. They are guarded, introverted and may distort
basic communications due to their emotional state. Sometimes they won’t tell you the truth. Sometimes they won’t tell
you anything. Although that creates difficulties for therapy, it also creates difficulties for the researcher trying to garner
information via face-to-face interviews.
In the classic studies by Kety et al. (1968, 1975), they included diagnoses of
schizophrenia sometimes derived from conversations between 5 and 20 minutes
in duration conducted through half-open doors. The data from these sparse
contacts were included in three broad categories: “outside the schizophrenic
spectrum,” “suspected schizophrenic spectrum,” and “schizophrenia.” They
were coded merely on disturbance of “emotional contact,” “language use,” and
“thought processes.” Any vague tensions or difficulties noted in the half-closed
door conversations could be counted as schizophrenia. The result was that any
and all “problems” were counted as schizophrenia, which increased the odds of
finding a higher relationship between one person’s problems and their relative’s
functional and emotional state. Kety et al. (1975) even fabricated some
interviews, in some cases including psychiatric records of people who had died,
thus being unavailable for face-to-face interviews.
A necessary part of demonstrating the genetic roots of any target behavior is using the scientific method to show that no
other factors can be contributing to or accounting for the differences. The researcher holds everything constant except
one factor (the independent variable) and measures the changes produced in the dependent variable(s). In these areas
of research, the assumption that the environments into which separated twins were placed are the same is called the
Equal Environment Assumption (EEA) or the “no selective placement assumption.”
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By either name, the EEA is required for good non-confounded scientific data, and it was assumed to be true by many
pro-genetic researchers. However, this assumption is shown to be violated in many specific studies and in the general
spirit of the times in which most of these initial split-twin studies were performed. This was because the spirit of the
times in the 1920s and 1930s was produced by the writings of men such as Galton, Irvine and Davenport, quoted above.
The notion was that biology is destiny. As Manfred Bleuler (1978) wrote:
“If one knows schizophrenics and their families well, it is sometimes a matter for despair to see how much they
suffer under the terrible concept of ‘familial tainting.’ Like a sinister shadow, it darkens the lives of many people
and entire families. The stifling uncertain fear of coming from an ‘inferior breed,’ of carrying within one’s self the
seeds of something pathological, morbid, and evil (I am speaking in the jargon the afflicted apply to themselves),
like a curse that you must pass on to someone else, causes oppressive feeling of inferiority” (p. 473).
Given the societal view that inferiors and failures were genetically programmed to fail, one must conclude that only
special kinds of people would be willing to adopt such troubled beings. In fact, the social services agencies involved with
these adoptions routinely included family history to prospective adopters unless the prospective adoptive parent
refused that information. That dissemination of knowledge with good or bad intent could produce circular and selfdefeating logic and reinforce the negative chances any adopted child would get very high-functioning parents or an
impartial, unbiased set of parents. Children with black marks in their charts would get heavy negative scrutiny from both
adoption agencies careful not to burden good people with problem children and from prospective adoptive parents,
who usually want “good” children.
Fortunately, Tienari’s research did focus on the effects of the adoptive parents’ functional levels on the adopted
children’s behaviors. He rated the adoptive families as a) “healthy,” b) “mildly disturbed,” c) “neurotic,” d) “rigid,
syntonic” or e) “severely disturbed.” His study showed “all” of the most severely disturbed adopted children were
reared in seriously disturbed adoptive families (Tienari et al., 1987, p. 482). His results and many others support more
environmental influence than genetic effect on later psychopathology.
Proband Method vs. Pairwise Method
The initial approach to researching similarities in twins involved identifying the twins, measuring the results, and simple
addition of the results. This is called the Pairwise Method. If both twins were diagnosed with schizophrenia in three out
of ten pairs, pairwise concordance for schizophrenia would be 3/10=30%. However, since the 1960s, a proband method
gained acceptance among several schizophrenia twin researchers. A “proband,” by their definition, is “a person through
whom other relatives are identified” (Johnson et. al., 2004, p. 165). Torrey et al. (1994) described the proband
procedure as follows: “In the proband method, a pair of twins concordant for schizophrenia is counted twice if each of
them was ascertained independently in the course of identifying subjects for the study.”
An example of this double counting is the following: If both twins are diagnosed in three of ten pairs, proband
concordance for schizophrenia would be 6/13 = 46% (3+3 out of 10+3). The pairwise method asks “In what proportion of
pairs are both called schizophrenic?” and the proband method asks “In what
proportion of probands is there a schizophrenic co-twin?” (Johnson et al., 2004, p.
166).
The proband method will always produce higher concordance results. If the researcher
is biased, this works in their favor. I liken the proband method to someone being able
to collect a winning lottery ticket prize any time you display it to any different store
owner – a never-ending jackpot! In one sense, this would be like having to go back to
jail and serve your criminal sentence every time someone else found out you have
been convicted of a crime. That process is multiple jeopardy, not just double jeopardy.
None of these make any sense. None of them occur anywhere else in the real world.
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In all of these studies, genetic similarity is confounded with environmental similarity. As the incidence of mental illness
varies with genetic similarity or dissimilarity, so too it varies with environmental similarity or dissimilarity. This holds true
for all of the characteristics listed above (schizophrenia, anger, intelligence, ADHD, etc.). The learned or environmental
components of the behavior can be easily identified. Let’s take paranoid schizophrenia, for example. Although Kallmann
and others don’t break down schizophrenia into schizophrenic subtypes, the author will do so for purposes of this
publication. We will use paranoid schizophrenia as the sample type because it is one of the most specifically manifested
schizophrenias. As mentioned earlier, most of the other subtypes mentioned in the current DSM (Disorganized, Residual
and Undifferentiated) are nonspecifically defined disorders.
Paranoid schizophrenics have delusions of grandeur and/or ideas of reference. They may hear voices and talk to
themselves. They may think people are out to get them. They talk aloud about “them,” and they talk back to them and
act upon them. They talk about the voices to their peers as well as to their children. They act out the dialogue in front of
their peers as well as their children. They can at times be severely incoherent, ranting and raving. They can be quite
impressive, even terrifying to adults, in their psychotic episodes.
And what are they teaching their children by example, i.e., Bandura’s modeling? They are teaching them high emotional
volatility, frequently demonstrating spouse and child abuse, inability to hold a steady job, inappropriate attitudes about
authority, and unusual associations of reference or persecution. A failed job interview is discussed in terms of the
interviewer’s race, religion or other possible attributes as the cause of the paranoid’s lack of employment, not the
paranoid’s paranoia. They rarely attribute the failed outcome of the interview to their bizarre associations,
hypersensitivity or emotional instability. They will also be creating high emotional levels in their children due to the high
stress that is created by the ranting and psychotic episodes.
Which children are most likely to be identically effected by these psychotic episodes? Those children of the same age
and same sex, since they will be cognitively at the same level of development to accurately or inaccurately understand
the false reality of the rants, reasons and excuses for domestic or child abuse. The most similar in age and cognitive
development are monozygotic twins.
Which children are most likely to be mistreated by the paranoid adult who is a parent? Again, their same age, same sex
children: the monozygotic children. That abuse can simply be from inappropriate expectations. Everyone, whether
normal or severely insane, has general expectations about children’s behavior. For a schizophrenic, these expectations –
reasonable or not – will be most similar for the same-sex,
same-age children. The two same-sex, same-age children
will be similarly treated or mistreated for the same
behaviors by the schizophrenic parent.
Let’s say the paranoid father has two identical twin boys
named Tom and Tad. Let’s say the paranoid father has a
ranting, raving outburst that kills the children’s mother.
Identical twin Tom will have lost a mother at the exact age
as his identical twin brother Tad. Tom will be put in
alternative care since his mother is dead and his father is
incarcerated. So will Tad. Tom will be very emotionally upset
by his the murder of his mother. So will Tad. Tad’s family
income will be diminished the same amount as Tom’s. The
only serious difference in the impact of this tragedy on Tad
vs. Tom is if one of them saw the murder happen and one
didn’t. Maybe Tom was in the back yard playing in the
sandbox oblivious to the sights and screams of murder while
Tad was in the kitchen trying to keep his father from killing
his mother.
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Genetics, Environment and Anger
Plomin et al. (1988) reported on emotionality in identical twins vs. fraternal twins who were either raised together or
raised apart. Their findings were as follows:
Raised Together
0.37
0.17
Identical Twins
Fraternal Twins
Raised Apart
0.33
0.09
These data show the consistent higher correlations of behavior between more genetically similar subjects. However,
note that the similarity of anger is reduced when the genetically similar people are raised in dissimilar environments.
In this table, the supposedly pure genetics of anger in identical twins raised together yield a correlation of 0.37. But
what environmental factors can be associated with their anger?
Looking at Bandura’s modeling theory again, one sees as early as 1965 that children imitate the behavior of the adults
and peers in their lives. Angry parents don’t just sit around being angry. They talk about it and they act angry in front of
their children. And what age/sex combination children are most likely to see the same episodes and comprehend those
episodes in the same way? The most genetically similar children, the monozygotic twins.
For example, take the case of a pair of dizygotic twins, one a girl and the other a
boy. The parents and society are likely to have different expectations of them. If
the male twin doesn’t make the football team, it may elicit different parental
reactions than if the daughter of the same age does not make the football team.
She probably won’t even be expected to try out for the team. If the female twin
wants to take ballerina lessons, she will probably be perceived differently than
the male twin who announces he wants to take ballerina lessons.
It is possible that the .33 correlation of the monozygotic twins’ emotionality is
not even all due to pure genetics? They have the highest similarity of
environment and perception of that environment; thus many of their similar
behaviors are shaped by similar environments. The angry adults are teaching all
of their children by modeling what to be angry about, how to talk about it, what
to do about it and whether to even become angry in the first place.
Let’s imagine a non-angry adult whose pen runs out of ink. She might quietly get
another pen or quietly ask someone else to get her one. When non-angry adults
have a hard day at work, they come home and do their socially defined homechores or help each other with shared tasks. In traditional households, the
mother may cook and the father may do the outside lawn work. Any tensions or
frustrations are likely to be worked out in a measured fashion. On the other hand, children with angrier parents are
learning by observation that when the ink pen runs out, the adult may curse, throw the pen across the room, blame the
child, blame the spouse, and make someone (maybe even the family dog) pay for it physically or emotionally.
It would be possible to go through other areas such as sexual orientation, intelligence, temperament, alcohol and drug
abuse, depression, attentional disorders, eating disorders, seasonal affective disorders, and criminal behaviors and
construct the same chart with their formative genetic and environmental components. Each of these areas will always
have the same question: how much of this was learned behavior and how much of it was inherited? The high correlation
of environment and genetics will always be the same. That overlap cannot be separated by the twin vs. non-twin
research methods that have been used so far.
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Good research into nature vs. nurture effects must clearly control for confounding factors; multivariate analyses can
separate the effects of those different variables. To design good research demonstrating that genetic effects – and
nothing but genetic effects – are causing a behavior, a researcher has to parcel out many factors, including but not
limited to the effects of:
a)
The twins being the same age: in general, families and societies expect and evaluate appropriateness based on
the age of a child. They expect more of children who are older; they expect less of children who are younger.
b) The twins being the same sex: families and societies may expect different things for different sexes. These are
sex-based stereotypes. Same-sex children are generally expected to behave in the same appropriate manner;
behaviors that are considered inappropriate will be similarly established for that culture, subculture or family.
c)
The twins being the same ethnicity: families, cultures and subcultures have prejudices. Even the experimenter’s
biases can be based on their and the subject’s ethnicity as well as the classic “Rosenthal” effect, in-thelaboratory-working-with-rats effect.
d) The twins being the same size: families, cultures and subcultures may have expectations of potential and
appropriate behaviors based on size alone. For example, Americans don’t expect dwarfs to be successful
professional basketball or football players and don’t chastise them if they aren’t. The American military didn’t
expect 6’4” inch soldiers to be tunnel rats during the Vietnam War.
e)
The twins being raised in the same socioeconomic class: each socioeconomic class has its “ins” and “outs,”
“do’s” and “don’ts.” Other socioeconomic classes do not necessarily accept those as normal. For example,
marijuana use was primarily in the entertainer subculture in America until it became popular among middle-and
upper-class “hippies” in the 1960s.
f)
The twins being raised in the same culture and/or subculture: some cultures believed that having sex with threeyear-old children was appropriate (Rush, 1991); most don’t.
g)
The twins usually having the same religious beliefs: some religions accept speaking in tongues; other religions
and mental health providers with other perspectives view speaking in tongues as psychotic.
h) The twins sharing the same prenatal environment, with toxins: some cognitive distortions can be produced by
teratogens (prenatal toxins). Many studies have demonstrated the effects of prenatal drugs on fetal
development.
i)
The twins sharing some amount of time together with their biological family before being adopted and therefore
have some exposure to all mutually learned pathologies.
j)
The twins being in the same “cohort” (same era in history-e.g., baby-boomers, hippies, yuppies, Gen-Xers, etc.).
k)
The twins having auditory hallucinations, but being diagnosed as schizophrenic when they are really Dissociated
Identity Disorder (Multiple Personality).
l)
Any psychopathology their adoptive parents might have.
m) The adoptive parents’ parenting methods.
n) Not considering abuse sequelae and PTSD as possible primary factors and true diagnoses in cases in which there
is overlap of symptomatology of ADHD, Bipolar, Schizophrenia or Depression. We know that severe abuse
produces severe emotional and cognitive distortions in anyone. We have no valid, unconfounded data that show
that any significant emotional lability or cognitive distortions are purely inherited.
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Genetics, Environment and Intelligence
Another topic in the genetic vs. environmental debate is the supposed inheritability of intelligence.
Researchers such as Sir Cyril Burt began publishing
studies on the inheritance of intelligence in the
early 1900s. Burt (1972) reported that Caucasians
as a group scored higher on intelligence test scores
than “Negroids” as a group. Those of undiscerning
purpose assumed that any Caucasian was smarter
than any Negroid.
Later researchers like Arthur Jensen (1970) and
Herrnstein and Murray (1994) continued to assert
that this group difference in average intelligence
test scores proves or indicates intellectual genetic
superiority of Caucasians over Blacks. Jensen (1970)
actually stated that 70% of intelligence was due to
genetic factors. Herrnstein and Murray (1994)
wrote that intelligence was largely (40-80%)
genetically heritable and that there were “racial
differences” in intelligence.
While it is factual that there has been a consistent
difference between Caucasian groups and Black
groups measured by these and other researchers,
that group difference does not mean that any one
Black individual or any other ethnic group member
is less or more intelligent than any Caucasian
individual.
More importantly, intelligence tests measure
current factual knowledge or lack thereof. No one
can assert that factual knowledge tests measure
some totally encompassing intelligence. However,
all psychological tests (intelligence, aptitude,
personality, psychopathology, etc.) are culturally biased. Other researchers have shown that cultural bias is the basis of
the test score differences between different racial groups (Gregory, 2007).
Robert L. Williams, II, Ph.D., produced the first demonstration and verification of the cultural bias by producing “The
Black Intelligence Test of Cultural Homogeneity” (1972). Dr. Williams is a St. Louis, Missouri psychologist and professor
emeritus. He derived a valid intelligence test using the St. Louis, Missouri, inner-city jargon of that time. It is a valid
intelligence test partly because it is a test of words, a component of most intelligence or aptitude tests, and it is normed.
He administered the instrument to groups of African-Americans and groups of Caucasians. His results showed an exact
10-point difference between groups but the difference was in favor of the African Americans. The African Americans had
higher IQ scores by 10 points as a group than the Caucasians.
Adrian Dove (1971) is a Black sociologist who developed an intelligence test of word comprehension called “The Chitling
Test.” Items from the test are shown on the following page.
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The Chitling Test
1. A “handkerchief head” is:
(a) a cool cat, (b) a porter, (c) an Uncle Tom, (d) a hoddi, (e) a preacher.
2. Which word is most out of place here?
(a) splib, (b) blood, (c) gray, (d) spook, (e) black.
3. A “gas head” is a person who has a:
(a) fast-moving car, (b) stable of “lace,” (c) “process,” (d) habit of stealing cars, (e) long jail record for arson.
4. “Bo Diddley” is a:
(a) game for children, (b) down-home cheap wine, (c)
down-home singer, (d) new dance, (e) Moejoe call.
5. “Hully Gully” came from:
(a) East Oakland, (b) Fillmore, (c) Watts, (d) Harlem,
(e) Motor City.
6. Cheap chitlings (not the kind you purchase at a frozen
food counter) will taste rubbery unless they are
cooked long enough. How soon can you quit cooking
them to eat and enjoy them?
(a) 45 minutes, (b) 2 hours, (c) 24 hours, (d) 1 week
(on a low flame), (e) 1 hour.
7. What are the “Dixie Hummingbirds?”
(a) part of the KKK, (b) a swamp disease, (c) a modern
gospel group, (d) a Mississippi Negro paramilitary
group, (e) Deacons.
8. If you throw the dice and 7 is showing on the top, what is facing down?
(a) 7, (b) snake eyes, (c) boxcars, (d) little Joes, (e) 11.
9. “Jet” is:
(a) an East Oakland motorcycle club, (b) one of the gangs in “West Side Story,” (c) a news and gossip magazine, (d) a
way of life for the very rich.
10. T-Bone Walker got famous for playing what?
(a) trombone, (b) piano, (c) “T-flute,” (d) guitar, (e) “hambone.”
As the reader can see, the Chitling Test is also based on African-American culture of that day. For the curious, the
answers are: 1. (c); 2. (c); 3. (c); 4. (c); 5. (c); 6. (c); 7. (c); 8. (a); 9. (c); 10. (d)
The Chitling Test group differences were also ten points between African Americans and Caucasians but the difference
was, again, in favor of the African Americans.
Americans of any race may do well on the Chitling Test due to cultural familiarity. Now I offer you an Australian
intelligence test (author unknown). It measures vocabulary, as do most intelligence tests. It also measures knowledge of
social propriety and coping with the environment as do many intelligence tests.
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The Original Australian Test of Intelligence
1. What number comes next in the sequence, one, two, three, __________?
2. How many lunar months are in a year?
3. As wallaby is to animal so cigarette is to __________
4. Three of the following items may be classified with salt-water crocodile. Which are they?
(a) Marine turtle
(b) brolga
(c) frilled lizard
(d) black snake
5. Which items may be classified with sugar?
(a) Honey
(b) witchetty grub
(c) flour
(d) water-lilies
6. We eat food and we __________ water.
7. Sam, Ben and Harry are sitting together. Sam faces Ben and Ben gives him a cigarette. Harry sits quietly with his back
to both Ben and Sam and contributes nothing to the animated conversation going on between Sam and Ben. One of
the men is Ben’s brother; the other is Ben’s sister’s child. Who is the nephew?
(a) Sam
(b) Harry
(c) Ben
8. Suppose your brother in his mid-forties dies unexpectedly. Would you attribute his death to:
(a) God
(b) Fate
(c) Germs
(d) No one
(e) Someone (f) Your brother himself
9. You are out in the bush with your wife and young children and you are all hungry. You have a rifle and bullets. You
see three animals all within range – a young emu, a large kangaroo and a small female wallaby. Which should you
shoot for food? (circle your answer)
(a) Young emu
(b) Large kangaroo
(c) Small female wallaby
10. Why should you be careful of your cousins?
Original Australian Test of Intelligence Scoring Sheet
The correct answers are:
1. One, two, three, many....the kuuk thaayorre system of counting only goes to three...thana, kuthir, pinalam, mong,
mong, mong, etc. The word mong is best translated as “many” since it can mean any number between 4 and 9 or 10
after which, or mong (many figures) would be more appropriate.
2. Those who say thirteen are right in European terms but irrelevant in Edward River terms. The speakers of kuuk
thaayorre clearly identify lunar menstruation and possess a notion of the lunar month as calculated as the time
between one phase of the moon and the next appearance of that particular phase. However, apart from having no
specific word to designate thirteen and thirteen only – yurr mong, or “very many” is the right answer. The annual
cycle is couched in terms of environmental rhythms rather than in terms of fixed, invariant divisions of time. The
“year” then is the time between the onset of one wet season and the onset of the next wet season – and wet
seasons may be early or late, so who can be precise?
3. The right answer is “tree.” This stems from the kuuk thaayorre speaker’s early experience with tobacco, which was
“stick” tobacco, hence it is classified with tree.
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4. Crocodiles, turtles, birds and frill necked lizards are all classified as minh (which broadly might be translated as
animals). Snakes – along with eels – are classified as yak, which may be broadly translated as snake-like creatures.
5. All the items are classified with sugar as belong to the class of objects known as “may.” Broadly translated, may
means vegetable food. Even witchetty grubs that are found in the roots of trees fall under this rubric – so does
honey, which is also associated with trees and hence fruit. The kuuk thaayorre language had no problem fitting flour
into the “may” category since it obviously resembled some of their own processed vegetable foods (e.g., yams like
Dioscorea sativa). The word “may” can also mean sweet and hence sugar, which of course does not resemble
anything in their traditional culinary repertoire.
6. “Eat” is the right word – well sort of. Where we make a distinction between “eating” and “drinking”, kuuk thaayorre
does not and they use the same verb to describe both functions and why not?
7. The clues are easy for kuuk thaayorre. An avoidance taboo operates between mother’s brother and sister’s son and
politeness requires that sister’s son should never directly face mother’s brother nor talk to him directly in company.
Sam and Ben are obviously brothers because of their unrestrained interaction while Harry, with his back turned to
both his uncles is obviously the respectful nephew.
8. Among the kuuk thaayorre God has been equated with a mythological character and he is definitely non-malevolent.
Both fate and germs are concepts foreign to the kuuk thaayorre belief system. No one dies without reason, and
suicide is unknown to him or her, so the right answer is SOMEONE – which is the case in this sorcery-riddled society.
9. The small female wallaby is the right answer. Emu is a food that may be consumed only by very old people.
Kangaroos, (especially large ones) may not be eaten by parents or their children. The children will get sick otherwise.
Everyone knows that....don’t they?
10. Some of them have to be avoided like the plague. For example, a male must avoid his father’s sister’s daughter, or
anyone classified with her. Such relations are called poison cousins in Aboriginal English.
Accessed from www.wilderdom.com/personality/intelligenceOriginalAustralian.html, April 4, 2010.
These items relate to the kuuk thaayorre tribe culture of the Edward River Community in Far North Queensland.
Any test, intelligence or otherwise, is culturally biased and only measures someone’s cultural familiarity. Intelligence – as
measured by intelligence tests – is only a measure of cultural familiarity, not a measure of innate intelligence that is
supposed to transfer to all skills, everywhere, anywhere.
Genetics, Environment and Alcoholism
Another supposedly inherited disorder is alcoholism. The pre-1960 perspective on alcoholism was that it was considered
a moral weakness. In the 1960s, for some reason, the excessive use of alcohol began getting promoted as an inherited
disease, not a moral weakness. That new perspective was supposed to make the alcoholic feel better about his or her
problem and be less stigmatized by society. This topic is covered here because its post-1950s research, while heavily
promoting the inherited disease nature of excessive alcohol consumption, also fails to account for many contributing
environmental variables in reaching the conclusion that it is genetically transferred.
Many of those studies used the “twin” study method done by Kendler (1988) and others cited in this paper. For
example, McGue and Iacono (2008) acknowledge that the twin study methods have their “critics,” but they also write
that “research has generally supported the validity of the twin study approach.” Others (e.g., Petronas et al., 2007) also
assume the similarities in the dependent variables between siblings and parents are genetic without assessing for
similarity of environmental influences, trauma, or modeling (vicarious learning).
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Oscar-Berman and Bowirrat (2005) note “Because selected dimensions of emotional temperament are associated with
distinct neurochemical substrates contributing to specific personality phenotypes, certain aspects of abnormal
emotional traits in alcoholics may be inherited” (p. 225). This writer hypothesizes that most of the abnormal emotional
traits in alcoholics and children of alcoholics are also learned.
For example, when a sober, non-abused adult’s ink printing system (pen or laser printer) runs out of ink, they put it in
the trash and find another ink pen or laser printer cartridge to continue their writing or printing. If any of their children
are observing them, they learn only a peaceful and quiet solution to the problem. On the other hand, when an alcoholic
adult runs out of ink, he may often get angry, curse, throw the pen, or hit the printer, blame it on someone else, hit
someone else or have some other emotional outburst and go look for a drink. The exhausted ink source becomes the
cause of their anger and something or somebody gets punished.
When a sober, non-abused parent wins the lottery, they feel positive, talk to others about what to do with the money,
and consider what they can do for other people with that money. Their children learn consideration and thoughtfulness.
When an alcoholic parent wins the lottery, they drink it away and then punish others when it’s all gone.
When the child of a sober, non-abused parent wants to participate in a sport, play a musical instrument or engage in
other prosocial activities, the nonalcoholic parent finds money for them to take the lessons and buy the equipment and
can soberly take them to and from the practices or events. Their children learn skills associated with caring for others.
Conversely, when the child of an alcoholic parent wants to play a sport, a musical instrument or participate in other
prosocial activities, the alcoholic parent doesn’t do those supportive things because they have spent all the money on
alcohol and they are too drunk to drive anyone anywhere. That child learns self-absorption and lack of caring, as well as
another reason to drink alcohol.
If not proband and not pairwise and not concordance, then what?
If the previously discussed paradigms that reportedly proved these disorders are inherited are not valid procedures,
what means or methods could actually be valid and acceptable for deciding if a mental illness is purely genetically
determined? What are the other possibilities for empirically demonstrating that any childhood, adolescent or adult
emotional, behavioral or cognitive disorder is genetically inherited? There is one independent method used to try to
establish this genetic causality lasting throughout life:
Show that the individual has been on one of the extremes of the normal distribution since birth. For example, test all
infants with an identical stimulus at birth on any physiological reactivity, such as heart rate lability or variance in EEG
spectrum measurements. If a cognitive, mental, emotional or behavioral disorder is purely genetic, the data should show
that more emotionally labile infants remain more emotionally labile as adolescents and adults without any
environmental changes, events or causes.
All natural phenomena occur along the “normal distribution” (Bell
Curve) when graphed. The Bell Curve shows that while some
people are above average on a trait, most people are near the
average and some other people are very low on the trait. For
example, in the world of physical traits some people of the same
age are very short, most of them are about average and some of
them are very tall. Sir Francis Galton did much of the early work
measuring physical traits. All people will fall somewhere along
that bell curve with physiological, cognitive or emotional levels.
This has been quantified in many ways across multiple research
studies. Once researchers have obtained relevant psychological data, they have to show that a person who is a highly
emotionally reactive or cognitively inappropriate person at base-rate measurement (for example, at age two) is still at
that extreme when measured again later in life.
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Has it been empirically confirmed that people with extremely low emotional reactivity at age one will be that same way
in relationship to their cohort group at a later age? Has it been empirically proven that highly emotionally reactive oneyear-olds will be highly emotionally volatile 20-year-olds? It is equivalent to assuming that the shortest newborns are
going to be the shortest 20-year-olds.
Are there any data that scientifically show a long-term relationship of birthday characteristics or any other infant
measures to the accurately predictable behaviors for the rest of life? Psychiatry has relied on the Kallmann-type analysis
for many of their studies. None of them have considered any interplay between genetics and environment. Studies that
tried to correlate physiological activity with complex mental processes were done by Ertl and Schafer (1969) and Hans
Eysenck (1982) and his colleagues (A.E. Hendrickson, 1982 & 1988). Their subjects were infants or children. These
researchers stimulated their subjects with auditory stimuli and measured various components of the auditory evoked
potential (AEP). They initially found correlations as high as +.77 between AEP total wave travel and intelligence scores.
This is an impressively high correlation between physiology and psychology. Unfortunately, many attempts to replicate
these initial significant correlations between cortical activity and intelligence failed, even in their own laboratories.
The only other current biochemically-based theory of schizophrenia from psychiatry (specific source or label
unidentifiable by the author) is one that assumes that the emotional difficulty may not be manifested at birth but lies
dormant until some environmental stress or emotional stress occurs during critical times in life, such as puberty. This is a
cousin of the theory that has been labeled the stress-diathesis hypothesis or stress-vulnerability model by Harrison
(1999) and Weinberger (1987). This approach assumes that one internal, biochemically-based problem (e.g.,
schizophrenia) interacts with another internal, biochemically-based
process (puberty) that is not apparent until the two biochemical
processes combine. However, these studies did not account for the
social and environmental changes that occur during puberty any better
than the twin-studies did.
For example, if schizophrenia is an interaction between that theorized
latent schizophrenia and puberty, one must also take into account what
new social demands and pressures the pubescent child faces. The
pubescent child faces all of the privileges and liabilities of growing up:
dating, sex, intimacy, the thrill of victory and the agony of defeat in
sports, relationships and work. The joy afforded by the greater
independence of adolescence initially overrides the demands to cope
well with it or fail. But does the failed adolescent or young adult revert
to the non-pubescent child? No, they are still pubescent with the same
urges and the same expectations of society and their peers that they
will try, try again and succeed the second time.
Sexual Abuse of the Chronically and Severely Mentally Ill
What about the incidence of physical, sexual or emotional abuse to schizophrenics? Did any of the classic “twin” studies
assess for abuses? No. Do any of the current studies on schizophrenia assess for abuse in them? Not many. Abuse and
neglect of any kind are severely under-examined in severe mental disorders.
I was acutely reminded of the abuse factor in schizophrenia while doing individual therapy with patients. One gentleman
had been diagnosed as paranoid schizophrenic, a diagnosis that has the poorest prognosis. As always, I asked him about
abuse. He said his father, whom he worshiped, would beat him every time they went fishing in their small johnboat. This
started when he was four. Repeated beatings in a small area by an adored figure might make a four-year-old 1)
excessively fearful, 2) excessively confused and 3) excessively distrustful. These three elements are the paranoid
schizophrenic’s entire basic syndrome.
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In another case, a paranoid schizophrenic’s family secrets were revealed quite accidentally. I had seen this middle-aged
man for several years but never got the secret from him. During treatment, his social and interpersonal interactions
improved over those of his merely-medicated state when he first came to therapy. One day an old farmer friend of mine
mentioned this man’s name, stating off-hand that this patient’s father had been a well-respected physician in town.
However, he (the farmer) knew that the physician had shot off one of his son’s toes with a pistol in a fit of rage, later
sewing it up and treating it without anyone finding out. This kind of secretive abuse led to his eventual mental illness. He
was not born with the excessive fear, paranoia and social incompetence. He was trained that way by the excessive anger
and abusiveness of his father.
Symptoms of a bipolar manic episode as described in the DSM-IV-TR could also possibly be produced by severe physical,
sexual, or emotional abuse. The actual criteria are the following:
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood, lasting at least 1 week (or
any duration if hospitalization is necessary).
B. Three (or more) of the following symptoms are persistent (four if the mood is only irritable) and have been
present to a significant degree:
1.
2.
3.
4.
5.
6.
7.
Inflated self-esteem or grandiosity
Decreased need for sleep
More talkative than usual or pressure to keep talking
Flight of ideas or subjective experience that thoughts are racing
Distractibility
Increase in goal-directed activity.
Excessive involvement in pleasurable activities that have a high potential for painful consequences
(e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments)
Abuse can produce all of the same symptoms: a distinct period of abnormally and persistently elevated, expansive, or
irritable mood, lasting at least 1 week (or any duration if hospitalization is necessary).
While this is considered a symptom of bipolar disorder, abuse victims can be triggered
(emotionally agitated) by here-and-now events that remind them of past abuses. This
author has seen emotional surges in combat veterans lasting for as long as a year in a
number of cases. The specific trigger for the one-year surges was when several Vietnam
combat veterans became battle-ready again after the terrorists rammed the planes into
the World Trade Centers and the Pentagon on 9/11/2001. Several of them went into
combat-vigilance, doing perimeter checks around their houses or farm acreage with
knives and fully loaded weapons. They even went back into combat-sleep routines (i.e.,
asleep three hours per night, accompanied by hypervigilance to external sounds). They
became over-reactive to sights, sounds and touches. They became irritable on a 24/7
basis. They all stood down only after our military attacked Afghanistan and Baghdad in
Operation Iraqi Freedom and Operation Enduring Freedom. They felt they could relax
because they felt someone was finally “in charge” (using a military solution to a military
problem). Many other combat vets from Vietnam and every other era also become
emotionally re-stimulated whenever America becomes involved in another armed
conflict.
Severely abused civilians, including those diagnosed with dissociative identity disorder, may become extremely
emotional when they are triggered by here-and-now reminders of their abuses. Therefore, an astute diagnostician
cannot and should not merely classify a person as manic or bipolar simply because they have severe emotional mood
swings.
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1. Inflated self-esteem or grandiosity. While many abused people have significantly low self-esteem, as Sigmund Freud
theorized, they can also have a pathologically elevated sense of self-esteem via the defense mechanism of conversion
reaction (i.e., that which is unacceptable is converted into its reverse phenomenon that is more socially and personally
acceptable). This can result from imitating abusers (introjections) or initiating a reaction formation on their insecurities.
Insecure, alcoholic people often have a “macho” front as a reaction formation to their true insecurity and feelings of
inferiority, shame, and failure. Therefore, a person should not be automatically diagnosed as manic or bipolar based on
the presence of these symptoms alone.
2. Decreased need for sleep. People in manic phases do have decreased need for sleep but so do people in triggered
trauma-based re-stimulations. The clinician should ask people who have trouble sleeping if they were ever abused, saw
or heard others being attacked in the dark or at night. If any of these happened, the individual may have paired the night
or darkness with pain, panic and possibly even death. Abuse can occur at night. It can occur in the dark. Many abused
people have difficulty shutting their eyes because that makes it dark. It makes them vulnerable. For many abused
people, darkness is not their friend. It has lost its soothing, calming properties by being paired with injury.
3. More talkative than usual or pressure to keep talking. Again, people in triggered trauma-related phases can exhibit
these behaviors. Some abused people even have a general style of rapid speech because they developed a coping
mechanism of trying to say the right things to please their abusers in order to avoid further abuse.
4. Flight of ideas or subjective experience that thoughts are racing. These are also manifested in a triggered abuse
victim. The adrenaline that stimulates the body also stimulates brain neurons.
5. Distractibility. This is the same as the hypervigilance of the PTSD victim. The adult hypervigilance may not be the same
as it was when they were being abused. Even after the abuser is dead, the abuse victim may be highly focused on hypermonitoring of the environment as a means of successful survival in adult life. All of these behaviors become so
automatic that the patient is not usually conscious of the basis of their hypervigilance without having undergone abuserelated therapy.
6. Increase in goal-directed activity. This can be the “flight into reality” pushed by a trauma victim’s attempts to prove
him or herself and combat the negative self-image the abuser and the abuses often produce in the trauma victim.
7. Excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., engaging in
unrestrained buying sprees, sexual indiscretions, or foolish business investments). Abused people with or without PTSD
often have “feelings of detachment or estrangement from others” (DSM-IV-TR, PTSD Criteria C [5], p. 468). An obvious
manifestation of such detachment can be seen when the abused child becomes detached, estranged and alienated from
their abusive adult caretaker. If this abuse is repeated by adult caretakers, the abused child may become guarded,
distrustful, fearful and contemptuous of all adult authority figures. This is because the child’s initial adult caretakers are
supposed to be knowing, wise and just within the child’s frame of reference. Repeated, unnecessarily harsh or abusive
discipline produces anger and resentment in the child. An example would be a child who was severely punished by his
mother and began hating her starting when he was six years old. This resentment at the pain inflicted by the
punishment generalizes first to resentment at the abuser and subsequently to any discipline meted out by any adult:
teacher, principal or judge.
If you control for all of those things and you still get a significantly high correlation or concordance pattern for
psychopathology like Kallmann and the others produced for schizophrenia or any of these other problems, then you
have shown that there is a significant genetic basis for the emotional disorder. The same criteria of all other
environmental factors listed in this paper would be required to show that any other behavioral abnormalities have
verifiable genetic components. No one to date has successfully completed this parceling out, and this author
hypothesizes the genetic effects on any behavior would be extremely small if they did. The only thing these studies have
shown is the effects that similar environments and environmental expectations produce on behaviors.
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Do Identical and Fraternal Twins Create Differing Environments?
Another effort to salvage the genetic cause of shared mental illness in genetically similar people appeared with the
writings by Manfred Bleuler (1955), son of Eugene Bleuler, the founder of the entire concept of schizophrenia. Shields
(1954), Kallmann (1958) and others also wrote about this. They all argued that identical twins are treated similarly
because their genes construct their environment, as opposed to the environment constructing their behaviors. Manfred
Bleuler wrote “Identical twins, on the basis of their common inherited predisposition, create for themselves on the
average a much more similar environment than is the case for the fraternal twins…the old idea that the environment of
twins varies without regard to their innate predisposition (Analge) is quiet erroneous; hence all further deductions which
used to be based on this premise must be wrong” (1955, p.3).
James Shields (1954) wrote “In so far as binovular (fraternal) twins are treated differently from one another and more
differently than uniovular (identical) twins, this is likely to be due, not so much to causes outside the twins as to innate
differences in the needs of the binovular (fraternal) twins themselves, manifested by different patterns of behavior” (pp.
239-240).
Later, Johnson at al. (2004, p. 71) wrote “Thus,
Shields took the main objection of the critics and
stood it on its head: the validity of drawing
genetic inferences from identical-fraternal
comparisons was now supported by the more
dissimilar environments ‘created’ by fraternal
twins.”
Kallmann (1958, p. 543) also wrote: “The popular
notion that the behavior patterns of the one-egg
(identical) twins are alike chiefly because of the
unusual similarity in their early environments has
yet to be substantiated. If confirmed, the
argument would only strengthen rather than
weaken any correctly formulated genetic theory.
Psychodynamic concepts, too, are built on the premise that man is selective in respect to important aspects of his life
experiences an (sic) so can be thought of as “creating his own environment” (emphasis added by J. Johnson).
Johnson et al. (2004, p. 72) continued “Kallmann was arguing that if identical twins’ more similar environments caused
them to behave more similarly, this ‘would only strengthen’ the genetic position!” As Johnson et al. also noted on the
same page, the dissident psychiatrist R. D. Laing commented “With this two-headed penny it is not clear how Kallmann
can lose” (1981, p. 143). Johnson et al. further commented that “But what is most conveniently forgotten is this:
according to this theory, twins’ parents must also be genetically predisposed (my emphasis) to manifest genetically
determined behavior and response modes.”
The above-mentioned “twins create their environments” argument suggests the children are genetically programmed to
act in lock-step with their genes, but that the parents’ genetic control is overwhelmed by their children’s behaviors. In
this argument, children have some supposed rigid, inborn propensity to display behaviors, while their parents’ actions
are characterized by plasticity and malleability. If parents can change their behaviors on the basis of environmental
factors as flexible, adaptive, effective behavior demands, it should follow that all children, including twins of any type,
can do likewise. As Johnson et al. note (2004, p. 73) “Yet children are portrayed as having a greater ability to change the
(genetically predisposed) behavior of adults than adults have to create, through their treatment (of their children),
similar behavior in identical twins (italics my addition).” It makes no logical sense to assume “a heads I win, tails you
lose” stance in scientific argument.
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Behavior Extremes Don’t Purely Call for Medication Remediation
Extreme behaviors, as Johnson et al. (2004) and others point out, do not always simply call for medication as the only
remedy. When a child manifests defiance or poor attention, there are many behavioral techniques available for
changing those behaviors besides drugs. These all involve applying negative consequences for undesirable behaviors and
positive ones for appropriate behaviors. For these consequences to be effective, the parent must be trained to deliver
them consistently and appropriately (Monastra, 2004; Barkley, 2000). Ineffective, confused parents produce ineffective,
confused, scattered children.
The uncritical attribution of genetics and biology to behaviors or emotional surges with clearly environmental aspects is
unacceptable because:
1) It reduces the responsibility of human agents (parents) to protect the vulnerable (their children) from the parent
or other predators.
2) It reduces the responsibility of caretakers to examine and admit their responsibility for the behavioral problems
of their children.
3) It has reduced the motivation and responsibility of an entire class of humans to keep striving (i.e., those on
disability because they believe they are and have been diagnosed as bipolar, therefore genetically doomed).
4) It disempowers those who are considered merely genetically or biochemically warped from receiving validation
of their emotional distress caused by brutalization.
5) It reduces the patient’s – and the mental health provider’s – efforts to search for deeper understanding of the
effects of the person’s maltreatment.
6) It has created a class of socially acceptable, legal drug addicts and made drug abuse extremely easy.
7) It has reified severe mental illness, reducing access for the chronically mentally ill to understanding about the
abusive people in their lives.
Every dollar allocated for psychotropic medication in the health care budget is a dollar taken away from helping the
patient or client learn about and change their mental illness-inducing environment. Joseph (2004) states that this
acceptance of genetic causality creates a “pessimistic” attitude toward society. He wrote:
“It is far easier to emphasize genetic predisposition than it is to create a society which ensures that
children do not grow up in seriously disturbed families. In this sense, the decision to emphasize genetic
endowment over environment is often based on vested interests and beliefs. It is not predestined that
disturbed families will always exist or that children will be forced to endure them. I am talking about
preventing psychological damage before it happens and not, as typically occurs in psychotherapy, simply
trying to undo damage that has already been done. Genetic and biological therapies in psychiatry tend to
blame the victim and let society off the hook, and in doing so, help support the social and political status
quo” (p. 163).
Although child protective services are still a lot better than they were when the first child protection laws were passed in
this country (1975), the author still sees children on a weekly basis that have been brutalized by fathers, mothers and
stepparents for years. I still see adults who have been brutalized by their parents after the child protection laws were
enacted. What else can we do to stop this slaughter of innocents and innocence?
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When mental health professionals diagnose,
they diagnose with an assumed etiology. It is
usually somewhere along the genetics vs.
environmental causation spectrum. The
literature reviewed here suggests that there is
no scientifically valid data that separate the
effects of environment and heredity in these
concordance studies of schizophrenia. There
are no scientifically valid data showing that any
mental illness is inherited, not even as a
predisposition. The data reviewed here suggest
that we need to stop assuming there are
inherited defects that produce mental and/or
behavioral disorders and work on preventing
the environmental causes of behavioral dysfunction. Those environmental factors include prenatal stresses (teratogens,
illegal drug use, physical abuse to the pregnant female, and overdose effects of legal drugs) as well as the known
childhood abuse and neglect contributors to behavioral and emotional abnormality. All of this critically reviewed
information changes the diagnostic and therapeutic approach from: “What is wrong with this person?” to “What has
happened to this person?”
Crime in the Genes: Natural Born Killers?
Many other writers besides Irvine (1903), quoted above, have speculated that “crime is genetic.” This hypothesis was
actually widely accepted long before adoption, twin or family studies were performed. The eugenist Charles Davenport
wrote:
“The acts of taking and keeping loose articles, of tearing away obstructions, to get at something desired,
of picking valuables out of holes and pockets, of assaulting a neighbor who has something desirable or
who has caused pain or who is in the way, of deserting a family and other relatives, of promiscuous
sexual relations-these are crimes for a twentieth century citizen but they are the normal acts of our
remove, ape-like ancestors…Imbecility and ‘criminalistic’ tendency can be traced back to the darkness or
remove generations in a way that forces us to conclude that these traits have come to use directly from
our animal ancestry and have never been got rid of…If we are to build up in America a society worth of
the species man then we must take such steps as will prevent the increase or even the perpetuation of
animalistic strains” (1911, pp. 262-263).
Another physician wrote:
“That a criminal father should beget a child pre-destined to criminality is a foregone conclusion” (Hall,
1914, p. 87).
Few current advocates of genetic determinism directly tout “genes for crime” since there are many other factors known
to contribute to criminal or antisocial behavior (poverty, illiteracy, child abuse). Some writers still argue that people
inherit predispositions for personalities that made them more likely to commit crimes. Goldsmith and Gottesman (1996,
p. 9) wrote:
“Notions such as “genes for crime” are nonsense, but the following notion is reasonable: There may be
partially genetically influenced predispositions for basic behavioral tendencies, such as impulsivity, that
in certain experiential contexts make the probability of committing certain crimes higher than for
individuals who possess lesser degrees of such behavioral tendencies.”
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The early Twin Method studies (e.g., Lange, 1930; Rosanoff, et al., 1934) that examined the relationship of criminal
behavior to genetic similarity found the same pattern (closer genetics were related to closer behavior similarity) as all
other methods using this paradigm. However, they are methodologically weak for all of the same reasons discussed in
this paper on the Twin Method for the other areas. Twins-Reared-Apart studies of criminality by Grove et al. (1990) also
suffer from the same methodological problem.
All of these studies that postulated an inherited predisposition of criminality also assumed that the original data
reporting that there were genetically-transmitted complex behaviors were valid. The critiques of those studies offered in
this paper suggest that the assumption of genetically transmitted criminal behavior is not valid, either due to similar
methodological errors or confusing biological similarity with environmental similarity.
More methodologically sound studies with larger samples sizes and without preselection for criminality – such as the
Scandinavian criminal twin studies by Christiansen (1977) and Dalgard and Kringlen (1976) – found no statistically
significant concordance based on genetic similarity. Dalgard and Kringlen concluded “These findings support the view
that hereditary factors are of no significant importance in the etiology of crime” (1976, p. 231).
Several writers (Pincus, 2001; Otnow-Lewis, 1998) even report specific cases of severely, sometimes serially-violent
criminals with the deadly combination of severe childhood abuse and brain damage. The severe physical and sexual
abuse generates massive emotionality and the brain-damage blocks the capacity of the prefrontal lobes to dampen that
emotion. While Widom (1989) found that 90% of people who have been physically abused do not become violent
criminals, Pincus (2001) wrote that 94% of the 150 murders he examined in a five-year period reported “frequent and
prolonged physical and sexual abuse.” None of the physical abuse, sexual abuse or brain damage was caused by
genetically-produced factors driving the individual into a predestined fit of rage. Environmental abuse interacted with
environmentally-produced neurological damage, not genetics, to produce this dance of murder for the perpetrators and
their victims.
In a review of neuroimaging research, Bufkin and Luttrell (2005) reported that about 100% of SPECT (single photon
emission computed tomography) and PET (positron emission tomography) studies reported deficits in prefrontal
functioning (frontal lobe deficits) in violent, aggressive, and antisocial groups. About 70% of SPECT and PET studies
reported deficits in temporal lobe dysfunction in violent groups, whereas about 100% of MRI studies reported deficits in
temporal lobes and amygdala functioning. Fabian (2009) listed the following as factors contributing to
neuropsychological impairment:
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Young maternal age during pregnancy
Maternal alcohol, nicotine, and/or drug use, and poor diet and medical care during pregnancy
Infant testing positive at birth
Low birth weight
Low heart rate at birth
Fetal maldevelopment, minor physical abnormalities, fetal alcohol syndrome
Pregnancy and birth complications
Parental criminality and substance abuse
Domestic violence to mother during pregnancy
Poor offspring nutrition and medical care
Large family size
Exposure to parental physical abuse and emotional neglect
Exposure to deplorable home conditions
Exposure to toxins, lead, parasites, infection
Poor socioeconomic conditions and deficient parental and offspring education
Substance abuse and dependence history
Experience of violent victimization that could include head injury and symptoms of PTSD
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Note that none of these factors is genetically transmitted. Note also Fabian’s glaring omission in not listing childhood
sexual abuse, which is present in most adult violent offenders and murderers.
Besides Fabian’s, Pincus’ and Otnow-Lewis’ data, the writer’s data also indicate prenatal drug abuse, malnutrition due to
the mother’s prenatal drug use, untreated post-natal jaundice and meconium stain are even more subtle contributors to
post-natal cognitive and impulse control problems. These findings will be presented in the author’s upcoming book titled
The Silent Slaughter (in press).
The scientific data suggest that the most violent offenders are made excessively emotional by environmental factors and
have nervous system damage from environmental factors. There are no valid studies that show extreme violence is
merely and completely genetically transmitted. For more comprehensive reviews of twin studies and antisocial
behaviors, see Eley et al. (1999) and Rowe, (1986). However, keep these current critiques in mind when reading them.
But what about “Real” DNA research?
The more up-to-date geneticist and molecular biologist may
criticize the old genetically-based research cited above as
only inferential, since none of it has dealt directly with
molecular biology, the analysis of DNA, RNA, and the rest of
the cellular structures we now know affect many aspects of
biological life and functioning. Watch the news through any
medium and one will hear almost monthly about newly
discovered genetic markers for any and all behavior or
mental disorders. Some, but not all, of these studies that
claim a link at the DNA level include Egeland, et al. (1987) for
bipolar disorders and Sherrington, et al. (1988) for
schizophrenic disorders.
More current articles are easily found at the touch of a search engine for genetic markers for depression (Caron and
Zhang, 2005), seasonal affective disorder (Provencio, 2008), and obesity by the Center for Disease Control (2010 at
www.cdc.gov/Features/obesity/) to name a few more. However, the author cautions the reader to critically analyze
articles claiming any genetic causation of complex human psychopathology from the new molecular-level geneticists in
light of the Fabian’s contributing factors listed above and the eight factors listed in the synthesis, below, before
assuming one has valid results about supporting the inherited basis of any complex behaviors.
Nature and Nurture: A Proposed Synthesis
Since Homo sapiens are comprised of both physical and mental processes, the writer proposes that any analysis for
understanding a complex mental health problem should utilize the following standards:
•
Always take both genetics and environment into account when assessing for diagnosis. Always use all three
perspectives of the biopsychosocial perspective to develop the diagnosis for any one individual.
•
Do not accept or generate a diagnosis that has not fully evaluated both genetic and environmental possibilities.
•
Do not accept or generate a diagnosis that has not used a broad-spectrum assessment device. For example, do
not accept a diagnosis of depression that was developed only using Beck’s Depression Inventory (Beck et al.,
1961) or ADHD using only something like McCarney’s (2004) Attention Deficit Disorders Evaluation Scale. There
is considerable overlap between symptoms across the board, be it organic vs. psychogenic, mental illness vs.
personality disorder, or one subclass of mental disorder vs. another subclass.
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•
Do not accept and do not generate any diagnosis that is not derived from national scientifically-based norms.
Most people have good days and bad days. Most people have strengths and weaknesses. However, at what
point are chemical and cognitive interventions warranted? There are as many responses to those questions as
there are respondents.
•
Parents have their standards of acceptable diagnosis and treatment, and teachers, lawyers, policemen and
children have others. The law defines the rights and responsibilities of each at any given time. Scientifically
normed tests give the most empirically-based, unbiased, impartial answers to most questions about how bad or
how much. The field of diagnosis and treatment can also benefit from those more objectively-defined levels and
limits.
•
Do not accept a diagnosis or data from the caregiver alone. Caregivers have their own subjective and partial
perspectives on the patient. Use reliable, impartial collateral informants whenever possible, such as teachers,
school counselors, foster parents, etc.
•
Do not assume that a disorder is caused by genetics just because there is familial history of similar behavior or
cognition. Environmental modeling of family similarities can be the cause.
•
Do not accept a diagnosis that does not inquire about abuses (sexual, physical and emotional).
•
Establish a national training program for biopsychosocial diagnosis and do not allow any unidemensionallytrained people to diagnose.
In closing, may the author be so bold as to hypothesize the following as an adequate explanation for most human
psychopathology:
Genetics merely esthetically determine what kind of gun the person looks like.
The childhood environment loads the gun, producing the psychological issues, cognitive problems and level of emotional
lability.
The adolescent and adult challenges and conflicts “pull the triggers,” activating emotional surges created by childhood
experiences or training.
About the Author:
Frederick W. Nolen, PhD, is a licensed psychologist who has a BA, MA and PhD from the University of Missouri-Columbia.
He was recognized as an expert witness by the courts of Missouri on combat PTSD in 1986 and recognized an expert on
Child Abuse: Victims and Perpetrators in 2005. Dr. Nolen has lectured extensively on Child Abuse and Neglect, Victims
and Perpetrators, Dissociative Identity Disorder (formerly known as Multiple Personality Disorder) and PTSD. He has
taught at colleges and universities in Missouri and Indiana.
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