obyvatel
The Living Force
Schizophrenia is a psychiatric disorder that has been studied quite extensively. Its prevalence rate is estimated to be around 1% in populations over the age of 18 years. It is believed that schizophrenia has a genetic component. Related to schizophrenia are personality disorders like schizoid and schizotypal disorders along with others which belong to the schizoid spectrum. Research on the cause (etiology) of schizophrenia has revealed some interesting insights. Here I will make an attempt to summarize the speculative theory put forward by Paul E Meehl, former professor of psychology in the University of Minnesotta. His publications are available at the university site (http://www.tc.umn.edu/~pemeehl/). I would also include some info on the schizoid and schizotypal personality disorders.
The question would come "why this topic?" I came across this topic while looking into schizoidal psychopathy in Political Ponerology. I was confused by some terms of a descriptive nature and wanted to see what was the basis of these terms. This is a complex topic - but I think it is worth getting a basic idea as it may have a pretty wide ranging effect on the population and is related to stuff we discuss here. I will be quoting and paraphrasing from Meehl's papers as well as other material.
Meehl's Theory
Schizophrenia involves both powerful genetic factors, and powerful environment factors. Any theory purporting to explain why some persons fall ill and others do not, that considers only one of these two classes of factors, is radically defective. Some humans have a talent for schizophrenia, just as some have a talent for playing the violin. But not everybody with violin talent becomes a violinist, and not everybody with a talent for schizophrenia becomes a schizophrene.
[quote author=Meehl]
Clinical schizophrenia (under which I include pseudo-neurotic as well as disintegrated degrees of decompensation) has a specific etiology, a sine qua non, a condition which is necessary but not sufficient for the production of the disease. This specific etiology I postulate to be a dominant gene, the ‘schizogene.’ Nobody can get schizophrenia if he lacks the schizogene, nobody in fact avoids schizotypy if he carries the schizogene, but many people — I postulate most, well over half — who carry the schizogene avoid schizophrenia, i.e., they remain compensated or at lease semi-compensated and at no point become psychiatrically diagnosable even by the currently enlarged standards of American psychiatry for the use of the schizophrenia label.”
[/quote]
So there is a dominant gene termed schizogene which is passed on through inheritance. Theorists and researchers have suggested that the milder pathologies, such as personality disorders, represent undeveloped or minimally expressed defective genes; for example, the schizoid personality may possess a schizophrenic genotype, but in this case the defective gene is weakened by the operation of beneficial modifying genes or favorable environmental experiences which would include life experiences as well as diet related factors ( gluten and schizophrenia ). Meehl’s theory includes a dominant schizogene with polygenic potentiators like introversion, anxiety, hypohedonia (lower ability to experience positive emotions) which can be treated as temperamental factors.
According to Meehl, a single dominant gene produces a basic cognitive and cognitive-emotional “slippage” by altering some function of the synapse at all points in the nervous system, but in an extremely subtle way. The term used is “hypokrisia” which means neural integrative defect or “insufficiency of separation, differentiation or discrimination”. This schizotaxic gene is “silent” in most cases and its owners cannot be identified on the basis of hallucinations or delusions.
Schizotaxia, Hypokrisia, Schizotypy
The term schizotaxia is coined by Meehl. It is derived from schizo - schism or break and ataxia - disturbance in arrangement, array, marshalling, ordering.
[quote author=Meehl]
I conjecture that whatever is wrong with the schizotaxic CNS (central nervous system) is ubiquitous, a functional aberration present throughout, operating everywhere from the sacral cord to the frontal lobes. More specifically, this “something wrong at all levels” is something wrong about the way individual neurons work, a functional parametric aberration of the synaptic control system. The integrative defect in schizotaxia is ubiquitous instead of being localized to cerebral subsystem defects.
[/quote]
As mentioned earlier, hypokrisia is the term used for this ubiquitous functional control problem at the level of synapses in a neuron. Meehl used the word "parametric" in this regard which indicates that it can be quantitatively bigger or smaller rather than a present or absent kind of situation. The word hypokrisia means an insufficiency of separation, differentiation, or discrimination.
Schizotypy is the resultant state of this defect. The form and content of this state is influenced by environmental conditioning and life experiences. So schizotypy is not inheritable but what is inheritable is schizotaxic central nervous system . Only a minority of persons with the CNS defect decompensate to the point of being diagnosable by psychiatric criteria. So in this respect most schizotypes are like men with the genome for gout who do not develop clinical gout throughout their entire life.
What is meant by hypokrisia or defect of integration?
[quote author=Meehl]
By saying that the defect is integrative, I mean that it is not a defect of input, storage, or retrieval, but it is analogous to (but different from) some other well recognized integrative defects: dyslexia, tone deafness, the specific spelling defect in some persons of normal intelligence and verbal ability, nonanatomic dysarticulation syndrome, attention deficit disorder, and perhaps some extreme degrees of poor motor control in persons free of neurological injury.
[/quote]
Why so many terms?
[quote author=Meehl]
I have been faulted for needless proliferation of language in distinguishing schizotaxia from schizotypy, since on my theory they are perfectly correlated in the population. Suffice it to point out that a correlated extension of two attributes does not collapse them into one attribute. As logician Quine likes to point out, the taxonomic fact that every animal with a heart has a kidney does not mean that the terms “heart” and “kidney” are synonyms to the biologist! Here we have different levels of analysis, one (schizotypy) in terms of psychisms, a second (schizotaxia) as an open concept about the integrative function of the brain, and a third (hypokrisia) as a specific conjecture about the neuron level process that underlies the schizotaxia. They are three distinguishable concepts, which is why a theorist could buy one of them and not the other two, or two of them and not the third. So we need a semantics adequate to discuss them.
[/quote]
Base Rates
Based on empirical statistical data about the incidence of schizophrenia and inheritance , Meehl hypothesizes that the rate of incidence of schizotypy is 10% . This is a high base rate. Meehl comments
[quote author=Meehl]
If one thoroughly assimilates Rado’s concept of schizotypy, and thinks about the fairly contented and highly achieving schizotypes like “Kepler and Newton, Calvin and Kant, Schiller and Rousseau, Erasmus and Spinoza, Whistler and Goldsmith, Wagner and Chopin, Robespierre and George Washington…” (Menninger, 1930, p. 76), matters appear differently. Naturally the schizotypes one knows as a clinician are more or less distressed, at least part of the time, or we wouldn’t find them in our practice. For someone with my views, who finds many schizotypal nonpatients among colleagues, neighbors, students, it seems evident that there are a lot of schizotypes who lead relatively contented and fulfilling lives, especially if their polygenic situation is favorable, (e.g., not too much anxiety parameter or hypohedonia), and if they have good fortune in their occupational choices and their choices of a mate.
[/quote]
How can such a high base rate be possible for a genetic defect through evolution when it is known from empirical data that diagnosed schizophrenes have low fertility rates? Shouldn't the deviant gene have long disappeared from the gene pool?
[quote author=Meehl]
Since schizotypy is not the same as schizophrenia, we cannot move directly from the impaired fertility of diagnosed schizophrenes to an equal impairment for schizotypes. The development of psychotic symptoms early in life is presumably a more severe impairer of reproductive fitness than merely having a schizoid personality makeup. It is well known that the fertility impairment is considerably lower in female schizophrenes than in males. I think a semicompensated female schizotype sometimes combines a certain carelessness about contraception with a special kind of erotic attractiveness (alluded to briefly in my 1962 paper), especially for neurotic males. In my 1962 paper I conjectured (although I have no quantitative support) that a plausible family constellation genetically for a schizophrene consists of a nonschizotypal father with anxiety or introverted polygenes, attracted to a compensated schizotypal mother, so that the proband gets the specific genetic loading from the mother’s side and the adverse polygenic potentiators from the father’s side.
If schizotypy had in past time some survival value for individuals, this could countervail a somewhat lower reproductive rate for those that survive. It has been suggested to me by a student that the narcissistic element of the schizotype could quite possibly have a survival value in the individual refusing to engage in group conflict such as war, raiding parties, etc., which are dangerous. Then there is a fairly good likelihood that in some preliterate cultures the shaman becomes so because of schizotypal characteristics such as hallucinations, dissociative tendencies, and the peculiar charisma of some bright, dominant schizotypes (Hitler, Wittgenstein). But I agree that this kind of speculation is dangerously ad hoc...
[/quote]
Decompensation of schizotypy
The link between schizophrenia and shamanic and messed up shamanic capacities based on diet has been discussed in a C session here . Meehl discusses (other) potent environmental factors that can cause decompensation of a schizotype.
[quote author=Meehl]
One can divide environmental influences into those that were operative during the formative period of the psyche and current stressors on the adult. The decline of the schizophrenogenic mother theory has led to dismissal of her theoretical importance, so I will go out on a limb and forecast that when we have better data, requiring high-validity personality measures, she will be found to play a causal role, and one larger than father. The most malignant parental pattern for male schizotypes is a dominant, controlling, hypohedonic, ambivalent, character armored, compensated schizotypal mother (who transmits the schizogene and provides an aversive reinforcement schedule) and an anxious, insecure, passive, introverted, ineffectual father (who transmits the potentiating polygenes and provides a poor role model and no protective buffering from mother). This combination is bad genetically and environmentally, and maximizes the probability of adult decompensation. As a colleague put it, harshly but conveying the family flavor, “The worst setup is a schizy battleaxe mother and a Caspar Milquetoast father.”
.....................
With some stretching of language, I subsume under the heading of “trauma” both major single traumata (e.g., childhood rape, witnessing violent death of a parent) and accumulative small traumata such as double bind rejections, unfavorable comparisons with preferred siblings, rejection by the peer group in school, effects of grinding poverty, and the like. I believe that cumulative small traumata or one major trauma raise the odds of adult decompensation. More broadly, I conjecture that almost any insult organic or social, suffices to raise the odds.
..........................
With regard to the precipitating stressors of adult life, I am inclined to lay great weight upon the “luck factor.” I agree with Sir Karl Popper that sheer luck, happenings that befall us that are not attributable even to some unconscious selection of our friends or occupations and which have nothing to do with the repetition compulsion, play a crucial role in human happiness, health, and achievement. Social scientists underestimate the sheer luck factor because it does not lend itself very readily to inclusion in our predictive and explanatory equations (Meehl, 1978, p. 811 and references cited thereat). The difference between a schizotype who wins the Pulitizer Prize for poetry, and his MZ twin who ends up as a chronic deteriorated schizophrene in the state hospital may not always be understandable by some kind of systematic factor of the sort that psychologists and sociologists are accustomed to putting into their equations, such as a strong parental preference for one twin, or one twin having been dropped on its head as a baby.
[/quote]
To be contd.
The question would come "why this topic?" I came across this topic while looking into schizoidal psychopathy in Political Ponerology. I was confused by some terms of a descriptive nature and wanted to see what was the basis of these terms. This is a complex topic - but I think it is worth getting a basic idea as it may have a pretty wide ranging effect on the population and is related to stuff we discuss here. I will be quoting and paraphrasing from Meehl's papers as well as other material.
Meehl's Theory
Schizophrenia involves both powerful genetic factors, and powerful environment factors. Any theory purporting to explain why some persons fall ill and others do not, that considers only one of these two classes of factors, is radically defective. Some humans have a talent for schizophrenia, just as some have a talent for playing the violin. But not everybody with violin talent becomes a violinist, and not everybody with a talent for schizophrenia becomes a schizophrene.
[quote author=Meehl]
Clinical schizophrenia (under which I include pseudo-neurotic as well as disintegrated degrees of decompensation) has a specific etiology, a sine qua non, a condition which is necessary but not sufficient for the production of the disease. This specific etiology I postulate to be a dominant gene, the ‘schizogene.’ Nobody can get schizophrenia if he lacks the schizogene, nobody in fact avoids schizotypy if he carries the schizogene, but many people — I postulate most, well over half — who carry the schizogene avoid schizophrenia, i.e., they remain compensated or at lease semi-compensated and at no point become psychiatrically diagnosable even by the currently enlarged standards of American psychiatry for the use of the schizophrenia label.”
[/quote]
So there is a dominant gene termed schizogene which is passed on through inheritance. Theorists and researchers have suggested that the milder pathologies, such as personality disorders, represent undeveloped or minimally expressed defective genes; for example, the schizoid personality may possess a schizophrenic genotype, but in this case the defective gene is weakened by the operation of beneficial modifying genes or favorable environmental experiences which would include life experiences as well as diet related factors ( gluten and schizophrenia ). Meehl’s theory includes a dominant schizogene with polygenic potentiators like introversion, anxiety, hypohedonia (lower ability to experience positive emotions) which can be treated as temperamental factors.
According to Meehl, a single dominant gene produces a basic cognitive and cognitive-emotional “slippage” by altering some function of the synapse at all points in the nervous system, but in an extremely subtle way. The term used is “hypokrisia” which means neural integrative defect or “insufficiency of separation, differentiation or discrimination”. This schizotaxic gene is “silent” in most cases and its owners cannot be identified on the basis of hallucinations or delusions.
Schizotaxia, Hypokrisia, Schizotypy
The term schizotaxia is coined by Meehl. It is derived from schizo - schism or break and ataxia - disturbance in arrangement, array, marshalling, ordering.
[quote author=Meehl]
I conjecture that whatever is wrong with the schizotaxic CNS (central nervous system) is ubiquitous, a functional aberration present throughout, operating everywhere from the sacral cord to the frontal lobes. More specifically, this “something wrong at all levels” is something wrong about the way individual neurons work, a functional parametric aberration of the synaptic control system. The integrative defect in schizotaxia is ubiquitous instead of being localized to cerebral subsystem defects.
[/quote]
As mentioned earlier, hypokrisia is the term used for this ubiquitous functional control problem at the level of synapses in a neuron. Meehl used the word "parametric" in this regard which indicates that it can be quantitatively bigger or smaller rather than a present or absent kind of situation. The word hypokrisia means an insufficiency of separation, differentiation, or discrimination.
Schizotypy is the resultant state of this defect. The form and content of this state is influenced by environmental conditioning and life experiences. So schizotypy is not inheritable but what is inheritable is schizotaxic central nervous system . Only a minority of persons with the CNS defect decompensate to the point of being diagnosable by psychiatric criteria. So in this respect most schizotypes are like men with the genome for gout who do not develop clinical gout throughout their entire life.
What is meant by hypokrisia or defect of integration?
[quote author=Meehl]
By saying that the defect is integrative, I mean that it is not a defect of input, storage, or retrieval, but it is analogous to (but different from) some other well recognized integrative defects: dyslexia, tone deafness, the specific spelling defect in some persons of normal intelligence and verbal ability, nonanatomic dysarticulation syndrome, attention deficit disorder, and perhaps some extreme degrees of poor motor control in persons free of neurological injury.
[/quote]
Why so many terms?
[quote author=Meehl]
I have been faulted for needless proliferation of language in distinguishing schizotaxia from schizotypy, since on my theory they are perfectly correlated in the population. Suffice it to point out that a correlated extension of two attributes does not collapse them into one attribute. As logician Quine likes to point out, the taxonomic fact that every animal with a heart has a kidney does not mean that the terms “heart” and “kidney” are synonyms to the biologist! Here we have different levels of analysis, one (schizotypy) in terms of psychisms, a second (schizotaxia) as an open concept about the integrative function of the brain, and a third (hypokrisia) as a specific conjecture about the neuron level process that underlies the schizotaxia. They are three distinguishable concepts, which is why a theorist could buy one of them and not the other two, or two of them and not the third. So we need a semantics adequate to discuss them.
[/quote]
Base Rates
Based on empirical statistical data about the incidence of schizophrenia and inheritance , Meehl hypothesizes that the rate of incidence of schizotypy is 10% . This is a high base rate. Meehl comments
[quote author=Meehl]
If one thoroughly assimilates Rado’s concept of schizotypy, and thinks about the fairly contented and highly achieving schizotypes like “Kepler and Newton, Calvin and Kant, Schiller and Rousseau, Erasmus and Spinoza, Whistler and Goldsmith, Wagner and Chopin, Robespierre and George Washington…” (Menninger, 1930, p. 76), matters appear differently. Naturally the schizotypes one knows as a clinician are more or less distressed, at least part of the time, or we wouldn’t find them in our practice. For someone with my views, who finds many schizotypal nonpatients among colleagues, neighbors, students, it seems evident that there are a lot of schizotypes who lead relatively contented and fulfilling lives, especially if their polygenic situation is favorable, (e.g., not too much anxiety parameter or hypohedonia), and if they have good fortune in their occupational choices and their choices of a mate.
[/quote]
How can such a high base rate be possible for a genetic defect through evolution when it is known from empirical data that diagnosed schizophrenes have low fertility rates? Shouldn't the deviant gene have long disappeared from the gene pool?
[quote author=Meehl]
Since schizotypy is not the same as schizophrenia, we cannot move directly from the impaired fertility of diagnosed schizophrenes to an equal impairment for schizotypes. The development of psychotic symptoms early in life is presumably a more severe impairer of reproductive fitness than merely having a schizoid personality makeup. It is well known that the fertility impairment is considerably lower in female schizophrenes than in males. I think a semicompensated female schizotype sometimes combines a certain carelessness about contraception with a special kind of erotic attractiveness (alluded to briefly in my 1962 paper), especially for neurotic males. In my 1962 paper I conjectured (although I have no quantitative support) that a plausible family constellation genetically for a schizophrene consists of a nonschizotypal father with anxiety or introverted polygenes, attracted to a compensated schizotypal mother, so that the proband gets the specific genetic loading from the mother’s side and the adverse polygenic potentiators from the father’s side.
If schizotypy had in past time some survival value for individuals, this could countervail a somewhat lower reproductive rate for those that survive. It has been suggested to me by a student that the narcissistic element of the schizotype could quite possibly have a survival value in the individual refusing to engage in group conflict such as war, raiding parties, etc., which are dangerous. Then there is a fairly good likelihood that in some preliterate cultures the shaman becomes so because of schizotypal characteristics such as hallucinations, dissociative tendencies, and the peculiar charisma of some bright, dominant schizotypes (Hitler, Wittgenstein). But I agree that this kind of speculation is dangerously ad hoc...
[/quote]
Decompensation of schizotypy
The link between schizophrenia and shamanic and messed up shamanic capacities based on diet has been discussed in a C session here . Meehl discusses (other) potent environmental factors that can cause decompensation of a schizotype.
[quote author=Meehl]
One can divide environmental influences into those that were operative during the formative period of the psyche and current stressors on the adult. The decline of the schizophrenogenic mother theory has led to dismissal of her theoretical importance, so I will go out on a limb and forecast that when we have better data, requiring high-validity personality measures, she will be found to play a causal role, and one larger than father. The most malignant parental pattern for male schizotypes is a dominant, controlling, hypohedonic, ambivalent, character armored, compensated schizotypal mother (who transmits the schizogene and provides an aversive reinforcement schedule) and an anxious, insecure, passive, introverted, ineffectual father (who transmits the potentiating polygenes and provides a poor role model and no protective buffering from mother). This combination is bad genetically and environmentally, and maximizes the probability of adult decompensation. As a colleague put it, harshly but conveying the family flavor, “The worst setup is a schizy battleaxe mother and a Caspar Milquetoast father.”
.....................
With some stretching of language, I subsume under the heading of “trauma” both major single traumata (e.g., childhood rape, witnessing violent death of a parent) and accumulative small traumata such as double bind rejections, unfavorable comparisons with preferred siblings, rejection by the peer group in school, effects of grinding poverty, and the like. I believe that cumulative small traumata or one major trauma raise the odds of adult decompensation. More broadly, I conjecture that almost any insult organic or social, suffices to raise the odds.
..........................
With regard to the precipitating stressors of adult life, I am inclined to lay great weight upon the “luck factor.” I agree with Sir Karl Popper that sheer luck, happenings that befall us that are not attributable even to some unconscious selection of our friends or occupations and which have nothing to do with the repetition compulsion, play a crucial role in human happiness, health, and achievement. Social scientists underestimate the sheer luck factor because it does not lend itself very readily to inclusion in our predictive and explanatory equations (Meehl, 1978, p. 811 and references cited thereat). The difference between a schizotype who wins the Pulitizer Prize for poetry, and his MZ twin who ends up as a chronic deteriorated schizophrene in the state hospital may not always be understandable by some kind of systematic factor of the sort that psychologists and sociologists are accustomed to putting into their equations, such as a strong parental preference for one twin, or one twin having been dropped on its head as a baby.
[/quote]
To be contd.
