The Turn of the Paradigm?:
Madness, Differential Sensitivity and
Early Life Experience
Andrew Moskowitz
Aarhus University
Kristiansand
4 June 2015
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A formative clinical experience
Outline of talk
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How do paradigms change?
What is the current, biomedical paradigm of
psychosis/mental illness?
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How well has it worked?
What could an alternative – socio-psycho-bio –
model of mental disorders look like?
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Supportive evidence
Diathesis/stress vs differential susceptibility
Early life experiences/disorganized attachment and a
possibly relation to delusions
Paradigms and psychopathology
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Current paradigm of mental illness,
emphasizing genetics and brain pathology,
has failed
An emerging trauma/dissociation/attachment
paradigm shows real promise
Such a paradigm may be supplemented by
conceptualizing individuals not as vulnerable
to negative influences, but as sensitive or
susceptible to environmental influences - for
better or worse
Thomas Kuhn and The Structure of
Scientific Revolutions (1962)
Kuhn’s argument

Science does not advance in a linear fashion

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Myth: More and more accurate data collected over time so that reality or
truth is more and more closely approximated
Rather, science always progresses under the influence of a dominant
paradigm
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Paradigm means
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a specific past scientific achievement held up as a model or exemplar and
the generally accepted beliefs and attitudes of a particular scientific community
A paradigm exerts an organizing influence on a field, determining to a large
extent
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what types of research questions are considered legitimate
and what sorts of answers are considered acceptable.
Ultimately, what is seen and what is not seen
Opposing paradigms in psychopathology
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Schizophrenia field
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Genetic/biologically
caused brain disease
Treatment is medications
or biomedical
technologies
Symptoms are
meaningless
(unconnected to life
contexts)
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Dissociative disorders
field
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DID is caused by
overwhelming severe,
often sadistic, childhood
trauma
Treatment is intensive
psychotherapy
Symptoms have meaning
and can be linked to life
events
DID almost never (and PTSD rarely) considered in any type
of schizophrenia research
Paradigmatic interpretation of voices

To schizophrenia field
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Voices (auditory verbal
hallucinations) are
biologically-generated
signs of brain disease
Content is meaningless
Treatment is medications
or distraction techniques
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To dissociative disorders field
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Voices are psychologicallygenerated indications of
unresolved loss or trauma
Content is meaningful
(split off aspects of the self/
parts of the personality)
Treatment involves engaging
these parts (which can be
challenging)

In other words, are psychotic symptoms, such as
delusions and auditory hallucinations

Random expressions of a diseased brain?
OR
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Encrypted communications of a tortured life?
We’ll first explore the former…
Basic assumptions of the
neo-Kraepelinian paradigm
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Dominant paradigm of mental disorders stems from
Emil Kraepelin
According to Klerman (1978), the neo-Kraepelinian
credo contains 9 propositions, 4 of which are:
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Psychiatry is a branch of medicine
There is a boundary between the normal and the sick
There are discrete mental illnesses… There is not one, but
many mental illnesses
The focus of psychiatric physicians should be particularly on
the biological aspects of mental illness
The idealization of Kraepelin
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Neo-Kraepelinian’s image of Kraepelin as an
objective scientist is flawed
Diagnostic cards, which formed the basis for his
classification system suffered from a ‘lack of
systematic rigour’, and served only to ‘supplement
and reinforce preconceived (diagnostic) concepts’
(Weber & Engstrom, 1987, pp. 382-383)
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Kraepelin is described as ‘fanatically’ working through
his cards over and over again, as though they were ‘rare
art objects’
These preconceived concepts were derived from
Kahlbaum and particularly, dementia paralytica or
general paresis of the insane
Emil Kraepelin and Dementia
Paralytica (General Paresis)
What was General Paresis of the Insane?
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A life threatening condition, rampant in early 19th century
Europe, that primarily struck young men, combining
psychotic symptoms (often grandiosity and impaired
judgment) with physical symptoms (including paralysis)
Suggested by Bayle (1822) to be linked to syphilis
By the late 19th century, this was largely confirmed
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Fournier, in 1893 and 1894 published a large series of cases (almost
50,000) in which GPI was overwhelmingly linked to syphilitic
infections (Kaplan, 2010)
He also used index cards to track these cases in ways that
foreshadowed Kraepelin’s use
By early 20th century, link between syphilis and GPI
confirmed by biological studies, leading to the only Nobel
Prize for a psychiatrist (Wagner-Jauregg)
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Who proposed malaria as a treatment!
General Paresis as the central paradigm
for Kraepelin
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‘All his life, he (Kraepelin) had a preoccupation, if not
obsession, with alcohol and syphilis… He had no doubt an
organic cause would be found for psychiatric illnesses and saw
general paresis of the insane as a template for the other illnesses’
(Kaplan, 2010, p.24).
‘General paresis was taken by Kraepelin to be the model disease
entity and he hoped that both schizophrenia and manicdepressive disorder would follow suit’ (Jablensky, 1995, p. 186).
As late as 1922, in the paper Ends and Means of Psychiatric
Research, Kraepelin continued to assert this
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‘(R)eaffirming the role of general paresis as his prototype, he declares his central
objective to be a “search for unitary morbid processes” which “always arise from
similar disease causes”… “what we require above all is a clear characterization of
the post-mortem appearances of the brain in as many morbid processes as
possible”’ (Shepherd, 1995, p. 191)
Post-mortem brain of a General Paresis of
the Insane (GPI) patient
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Model disease entity
for Kraepelin (and
neo-Kraepelinians) is
Dementia Paralytica
(GPI) caused by
advanced syphilitic
infections
A genuine neuropsychiatric disorder!
General paresis as the exemplar for the
neo-Kraepelinian paradigm
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‘The example of General Paresis, with the assumption not
only that mental disorders were brain disorders, but that
any classification of psychopathology was best pursued
through identifying brain pathology, not only drove
Kraepelin’s typology, but also still underpins that of the
current diagnostic systems influenced by his thinking’
(Moskowitz, 2011, p. 350)

Gottesman & Shields, prominent psychiatric genetic researchers
allied with the neo-Kraepelinians wrote in 1973 of coveting for
schizophrenia the solid genetic grounding of ‘pellegra, paresis,
tuberculosis, polio, and PKU’ (p. 15)
The importance of Kraeplin’s
fundamental dichotomy
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The neo-Kraepelinians championed Kraepelin’s
greatest achievement - the distinction between
dementia praecox (schizophrenia) and manicdepression (bipolar disorder) - as the cornerstone of
their diagnostic system
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‘…if the twin pillars of manic-depressive psychosis and
schizophrenia are disturbed before there is anything better
to put in their place, the roof will come crashing down’
(Kendell, 1987, p. 500)
Paradigms and Anomalies
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According to Kuhn, problems arise for paradigms
when no acceptable answers are generated for issues
considered fundamental
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This, along with too many or too important anomalies,
pushes a paradigm toward a crisis
Anomalies
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Results not compatible with dominant paradigm occur
Example: CERN experiments demonstrating neutrinos
traveling faster than the speed of light - not predicted by
Einstein’s theory
usually ignored or adjustments made to keep fit with
paradigm
Scientific Revolutions
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A scientific revolution occurs when an
alternative paradigm is proposed that
explains some of the anomalies as well
as most previous findings
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Revolutions do not occur in the absence of a
suitable alternative paradigm
Kuhn suggests that for some revolutions to
occur, the ‘old guard’ (‘power elite’) has to ‘die
out’!
Failures of the neo-Kraepelinian paradigm:
schizoaffective disorder
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Evidence now suggests that schizoaffective disorder
is a valid disorder (Marneros & Akiskal, 2007)
A disorder between schizophrenia and bipolar
disorder was not predicted by Kraepelin, and poses a
major challenge for the paradigm
A dimension is implied, on the basis of family
studies and many other factors
Paradigm response?
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Calls to eliminate schizoaffective disorder. DSM-5
criteria for schizoaffective disorder are even narrower
than the DSM-IV.
Failures of the neo-Kraepelinian paradigm: nonspecificity of schizophrenic (psychotic) symptoms
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Increasing evidence that psychotic symptoms are common in the
‘normal’ population and do not differ in nature from those found
in schizophrenia (Murphy et al, 2010;Van Os et al, 2008,)
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Other factors determine symptom persistence and psychiatric diagnosis
Psychotic symptoms are common in many disorders, including
PTSD (Shevlin et al, 2010), and are not always clearly related in
content to the trauma (Scott et al, 2007).
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‘Psychotic experience is to the diagnosis of mental illness as fever is to the
diagnosis of infection – important but non-decisive in differential
diagnosis’ (Fischer & Carpenter, 2009, p. 2081)
Failures of the neo-Kraepelinian paradigm:
antipsychotic medications
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Are less effective than previously believed,
have more serious side effects and do not act
directly on psychotic symptoms
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‘(A)ntipsychotics do not primarily change thoughts
or ideas; instead, they provide a neurochemical
mileau wherein new aberrant saliences are less
likely to form and previously aberrant saliences are
more likely to extinguish… antipsychotics lessen
the salience of the concerns, and the patient “works
through” her symptoms toward a psychological
resolution’ (Kapur, 2003, p. 17)
Failures of the neo-Kraepelinian paradigm:
genetic findings
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Significant overlap between schizophrenia and bipolar disorder
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‘new work provides compelling support for the… evidence that
schizophrenia and bipolar disorder partially share a common genetic
etiology’ (Craddock et al, 2008, p. 483)
‘genetic studies point to a shared neurobiology across the two disorders’
(Thaker, 2008, p. 720)
Questionable validity of previously cited genetic findings
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A large scale, well-designed study found ‘none of the (genetic)
polymorphisms were associated with the schizophrenia phenotype at a
reasonable threshold for statistical significance’ (Sanders et al, 2008, p. 421)
‘The project to ground our messy psychiatric categories in genes… may be
in fundamental trouble’ (Kendler, 2006, p. 1145).
‘The historical effort to ground the categorical nature of schizophrenia in
genetic theory has failed’ (Kendler, 2014, p. 5)
The dominant paradigm’s response to crisis?
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Moving the goal posts…
‘As the neo-Kraepelinian edifice begins to crumble, adherents resort to stronger
and stronger biological language, as though words such as neuropsychiatry and
endophenotypes had the power to restore its once shining façade. The emphasis on
endophenotypes… involves exploring putative underlying biological variables that
may have only an indirect relationship to the signs and symptoms of mental
disorders. For example, … apparent genetic impairments in memory and
intelligence as conveying liability for schizophrenia (Toulopoulou et al., 2010).
The strong emphasis on endophenotypes, arising from a failure to find clear
connections between genetic makeup and psychiatric diagnoses or symptoms,
suggests that the neo-Kraepelinian stalwarts have beaten a strategic retreat; at the
same time that psychological approaches to treating and understanding psychiatric
symptoms, including delusions and hallucinations, have made great strides, the
dominant paradigm has given up the traditional territory of mental disorders—the
signs and symptoms that people suffer from and that treatments target’.
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‘So, the neo-Kraepelinian, categorical, medically based diagnostic system clearly
seems to be in a state of crisis. But, as Kuhn has noted, a discipline such as psychopathology will not loosen its grip on a paradigm unless a suitable alternative is available to take its place. What is the evidence that one is appearing?’ (Moskowitz, 2011)
The seed planted in the DSM-III
The emerging attachment/trauma/
dissociation paradigm
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Insecure attachment patterns, and particularly disorganized attachment, greatly
increases the likelihood of a range of mental disorders, including schizophrenia
(Liotti & Gumley, 2008)
Childhood trauma, and aversive childhood experiences, change the structure and
functioning of the brain in powerful ways – ways that have previously been seen as
evidence for a neurobiological disorder (Read, Fosse, Moskowitz & Perry, 2014)
Childhood trauma strongly predicts a wide range of mental disorders
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A prominent psychiatric geneticist, Kenneth Kendler, concluded from a large-scale twin
study that childhood sexual abuse was ‘causally related’ to the development of psychiatric
and substance abuse disorders (Kendler et al, 2000, p. 953), and that this relationship (at
least for major depression) was ‘much stronger’ than for any gene linked to schizophrenia or
bipolar disorder (Kendler, 2006, p. 1140)
In addition, there is now extensive evidence, from a range of studies, that childhood trauma
specifically predicts psychotic symptoms
Dissociation plays a central role not only in DID, but also in PTSD, BPD and
possibly schizophrenia (certainly in auditory hallucinations)
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There may be a range of ‘dissociative’ and ‘non-dissociative’ disorders, or ‘cohesive’ and
‘non-cohesive’ (ego) disorders
The emerging attachment/trauma/dissociation
paradigm: genetics and brain development
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Family patterns of psychosis formerly attributed to genetics may be
explained by trauma. A large scale case-control and case-sibling
comparison concluded:
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‘Discordance in psychotic illness across related individuals can be traced to
differential exposure to trauma.… Positive psychotic symptoms in vulnerable
individuals may arise as a consequence of the level and frequency of exposure to
abuse’ (Heins, et al, 2011, American Journal of Psychiatry)
Plus the limited genetic evidence that exists is at least partly gene x
environment evidence. The field of epigenetics emphasizes the powerful
impact of the environment on the expression of genes.
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‘(R)odent and non-human primate studies replicate the vulnerability of the prefrontal
cortex, amygdala, hippocampus, and HPA axis to early-life adversity…’ (Roth And
Sweatt, 2011a)
‘To the extent that an increased incidence of schizophrenia is associated with earlylife adversity, epigenetic changes triggered in early prenatal or postnatal
developments might predispose the development of schizophrenia later in life’ (Roth
and Sweatt, 2011a)
The hippocampus and childhood trauma
The hippocampus,
which is very
important for
episodic memory
and integrative
functions, is
powerfully
affected by
chronic stress,
particularly in
childhood.
Teicher et al (2012), on childhood
maltreatment and the hippocampus
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‘…the most intriguing finding to emerge from
this study was evidence for maltreatmentrelated alterations in the subiculum [of the
hippocampus], given the importance of this
region in the regulation of the HPA axis,
dopaminergic responses to stress, and risk for
substance abuse and psychosis’ (Teicher et al,
2012)
The emerging attachment/trauma/dissociation
paradigm: treatment
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Psychotherapy is effective treatment for psychotic symptoms
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And can prevent the development of psychotic disorders, including
schizophrenia (French et al, 2007, Lemos-Giráldez, 2009)
Trauma-based therapies are particularly important
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‘Our findings that childhood abuse can influence the content of
psychotic symptoms, (suggests) that it is important to assess
childhood trauma and trauma-related symptoms in patients diagnosed
with psychosis, and to offer a range of treatment options that include
trauma-relevant interventions’ (Rieff et al, 2010, p. 363)
Van der Berg & Van der Gaag (2012) found that EMDR reduced
delusions and some auditory hallucinations in persons with comorbid
PTSD and psychosis - even without psychotic symptoms being
directly targeted
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A subsequent study found delusions, but not auditory hallucinations, to improve
One further turn of the paradigm
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Are those who become labeled mentally ill
inherently defective, or potentially superior?
Are they vulnerable because of an inherent
weakness, or more sensitive to influence than
others - for worse or for better?
Vulnerability to harm vs sensitivity to
influence
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A number of researchers are now suggesting, on the basis of
evolutionary theory and empirical research, that some people
are more sensitive, for better or for worse, than others.
Certain gene alleles (dopamine, serotonin, etc.) may
predispose to this
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Differential susceptibility (Belsky & Pluess)
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Sensory processing sensitivity (Aron & Aron)
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Personality type (15-20% in many species) processes sensory
information deeply before acting
Biological sensitivity to context (Boyce & Ellis)
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Differences within families are normal and evolutionarily logical
Highly supportive or highly aversive environments (including prenatal)
increase stress sensitivity/physiological reactivity
Differential sensitivity
Classic diathesis (vulnerability) –
stress model
‘Beyond Diathesis Stress: Differential susceptibility to
environmental influences’ (Belsky & Pluess, 2009)
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‘The central thesis in this paper… is that those putatively
“vulnerable” individuals most adversely affected by many kinds
of stressor may be the very same ones who reap the most benefit
from environmental support and enrichment, including the
absence of adversity’. (p. 886)
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This appears to apply not only to children with a difficult temperament,
but also to those with genetic variants of the serotonergic and
dopaminergic systems (linked to sensitivity to stress), previously seen as
indicators of vulnerability to psychosis.
Interventions to improve parenting differentially affect the behavior of the
more sensitive children (with a specific dopamine gene allele). Poor
parenting led to most ‘externalizing behavior’ and sensitivity to stress,
while good parenting led to the least. (Van IJzendoorn et al, 2008)
Differential susceptibility (sensitivity)
model (Ellis et al, 2011)
From Bakermans-Kranenburg & Van
IJzendoorn (2011) intervention study
Time for a paradigm switch?
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Current ‘medical’ model, neo-Kraepelinian or biopsychosocial (‘biobio-bio’) paradigm has explained little and been faced with numerous
‘anomolies’
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New paradigm emphasizing sensitivity (not vulnerability), adverse life
experiences - trauma, attachment - and dissociation, better explains
current findings - including biomedical ones and
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Makes evolutionary sense!
Social support for a new paradigm
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Is in a current state of crisis
Voice hearing/user/family movements
Journalistic critiques of psychopharmacology and medical model
Increasing acceptance of high-ranking journals of publications consistent
with a new paradigm
What to call it?
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Socio-psycho-biological paradigm?
Delusions and early attachment
experiences
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Could delusions - paranoid, grandiose,
delusions of reference - be related to early
disturbed attachment experiences?
Delusions in schizophrenia and
emotional arousal
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Delusional ‘mood’ or ‘atmosphere’ (‘pre-delusional state’)
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Edinburgh High Risk Schizophrenia study (Cunningham Owens et al,
2005)
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Depression and anxiety very common in psychotic prodrome (Yung and
McGorry, 1996)
Other intense mood states – including love and joy – possible (Watts, 2007)
Perplexity and foreboding also common (Watts, 2007)
‘Considerable degrees’ of anxiety and depression in high risk sample,
particularly in subgroup which later became psychotic
anxiety and depression decreased with the development of psychosis
‘anxiety-type phenomena may partially remit as psychotic features escalate’ (p.
390)
Thus, delusions may serve to bind or reduce anxiety or other powerful
emotions
Could some intense affective experiences preceding delusions be
memory-related, but not recognized as such?
Jaspers’ (1913) classification of delusions
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Karl Jaspers argued that some delusions were clear
explanations for an experience (such as somatic
hallucinations)
He called these secondary delusions, and argued that they
were not specific to schizophrenia
Secondary delusions may be, for example, explanations for
flashback-related hallucinations, which are not recognized as
memory related
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Sexual abuse survivor’s delusion of ‘snakes in my bed’
Such delusions may serve a defensive purpose - to keep the traumatic
memories from reaching consciousness
Similar to avoidance in PTSD and compartmentalization in
personality parts in DID (which may not be possible for psychotic
disorders)
Jasper’s Primary delusions
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But Jasper also described another form of
delusion - primary delusions
He argued that these were psychologically
irreducible or un-understandable
Concern was with the form or experience of
the delusion, not with its content
But delusions did not arise out of the blue, but
out of a typical affective state
Jaspers on Delusional atmosphere (‘Wahnstimmung’) preceding primary delusions
‘We find that there arise in the patient certain primary sensations, vital
feelings, moods, awarenesses: “Something is going on; do tell me what on
earth is going on!”… Patients feel uncanny and that there is something
suspicious afoot. Everything gets a new meaning. The environment is
somehow different – not to a gross degree – perception is unaltered in itself
but there is some change which envelops everything with a subtle, pervasive
and strangely uncertain light. A living room which was previously felt as
neutral or friendly now becomes dominated by some indefinable atmosphere.
Something seems in the air which the patient cannot account for, a distrustful,
uncomfortable, uncanny tension invades him…This general delusional
atmosphere with all its vagueness of content must be unbearable. Patients
obviously suffer terribly under it and to reach some definite idea at last is like
being relieved from some enormous burden.’ (Jaspers, 1913/1963, p. 98).

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Jasper’s ‘uncanny’ is the German ‘unheimlich’
An unusual clue from an obscure Freud essay…
Freud’s (1919) analysis of feeling
‘uncanny’ (‘unheimlich’)

‘Heimlich’
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‘From the idea of “homelike”, “belonging to the house”, the further
idea is developed of something withdrawn from the eye of
strangers, something concealed, secret’ (p. 225).
Freud argued that Heimlich could be transformed into its
opposite Unheimlich
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He quotes Schelling to say: “‘Unheimlich” is the name for
everything that ought to have remained . . . secret and hidden but
has come to light’ (p. 224).
Freud argued that the feeling of uncanniness related to ‘secretly
familiar’ (p. 245) infantile experiences that had been repressed but
that had been ‘once more revived by some impression’ (p. 249).
The original feeling need not have been negative; the uncanniness
is due to the uncalled-for repetition, the re-emergence of the
familiar in an unfamiliar context
A speculative association of early attachment
experiences with Wahnstimmung

Disturbing attachment experiences from the 1st few months of life, particularly those
associated with disorganized attachment (parent as frightening or frightened), can be
stored as emotional memories (because the amygdala is active), but without any
autobiographical context (because the hippocampus is not yet fully functional).
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There is some evidence that disorganized attachment (followed by a dismissing attachment
style) may be related to schizophrenia
Such emotional memories would likely share many components with Wahnstimmung
- including fear, confusion, and foreboding
In addition, early attachment memories can include rudimentary conceptions of self
and other - as perpetrator, victim or rescuer - which could underlie subsequent
paranoid or grandiose delusions
Such decontextualized affective states could be triggered by situations somehow
reminiscent of these early attachment situations, or perhaps simply by the activation
of the attachment system, in a special context
These experiences cannot be recalled as memories (and thus need not be repressed or
dissociated), because the autobiographical memory system/hippocampus is not fully
active before age two
The trajectory from early attachment
experiences to psychopathology
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Disorganized attachment has also been linked to
DID and Borderline Personality Disorder
Liotti (2009) speculates that subsequent childhood
trauma is required for DID
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Emotional abuse and neglect emphasized more in
psychosis research
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Clinical experience supports this
Than sexual abuse
Differences in the type of trauma across groups?
Perhaps also capacity for dissociation differs?

Delusions are needed when dissociation is limited?
Are we witnessing a turn of the paradigm?
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Perhaps…
Will only happen if
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Delusion that brain studies can explain everything is
overcome
Delusion that those diagnosed with mental disorders are
fundamentally different from the rest of us is overcome
Fear of PTSD and dissociative disorders by psychosis
field is overcome

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And this conference is a great start!
More careful longitudinal studies are conducted
Clinically

More approaches from trauma and dissociation field
should be tried with psychotic disorders
‘You think you’re better than us,
don’t you? You think this could
never happen to you’…
The last word from Carl Jung’s (1908)
The Content of the Psychoses
‘(W)e can maintain with complete
assurance that in dementia praecox
there is no symptom which could be
described as psychologically
groundless or meaningless. Even the
most absurd things are nothing other
than symbols for thoughts which are
not only understandable in human
terms, but dwell in every human
breast. In insanity, we do not discover
anything new and unknown; we are
looking at the foundations of our own
being, the matrix of those vital
problems on which we are all
engaged.’