Posts Tagged ‘schizophrenia’
Posted on October 8, 2010 - by David
I am working directly from the unpublished text of Liah Greenfeld’s forthcoming book, Mind, Madness, and Modernity: The Impact of Culture on Human Experience. All the original ideas, and all interpretations and analysis of primary and secondary source materials used to support the ideas are attributable to Liah Greenfeld. Read the introduction to the exposition here.
part 3 – Madness: A Modern Phenomenon
In this last installment, we consider how Greenfeld’s theory of the mind makes it possible to see schizophrenia and manic-depressive illness (that is, major depression and bipolar disorder), which are usually considered distinct disorders, as diseases of the will, existing on a continuum of complexity of the will-impairment experienced.
Culture – the symbolic transmission of human ways of life- is an emergent phenomenon, a new reality with its own rules, that nonetheless operates within the boundary conditions of life. This symbolic reality is only alive, (the process can only occur), in individual brains, hence the understanding of the mind as “culture in the brain,” or “individualized culture.” As described in part 2, three important “structures” of the mind – (patterned and systematic symbolic processes which must be supported by corresponding patterned and systematic processes in the brain) – are identity, will, and the thinking self.
Identity - the relationally constituted self – is always a reflection of a particular cultural environment. Greenfeld hypothesizes that the lack of direction given by modern culture makes the once relatively simple process of identity formation much more complicated. A well formed identity is able to subjectively rank the choices present at any moment, giving the will, (or acting self), a basis for decision-making. It follows then that problems with identity formation lead to problems with the will. Malformation of identity and impairment of the will necessarily affect the functioning of the thinking self (the “I of self-consciousness”) – the part of the mind which is explicitly symbolic in the sense that it operates with formal symbols – above all, language. The thinking self may become fixed on questions of identity; it may have to stand in for the will, when a person has to talk him/herself into acting in situations which normally wouldn’t require self-conscious reflection (e.g going to the bathroom, eating, getting out of bed); or in the most severe cases, the thinking self may become completely disconnected from individualized culture, in which case all the cultural resources of the mind range free, without direction from identity and will.
The experiences of those who suffer from mental illness begin to make sense within this framework. In major depression, the will is impaired in its motivating function – the ability to force oneself to act or think as one would like to, or as would seem appropriate, is severely lessened. The mind at this stage remains individualized and one has a definite, though distorted and painful, sense of self. The thinking self becomes negatively obsessed with identity, and an incredible dialogue of self-loathing thoughts takes hold. It is insufferable to be oneself, and death naturally suggests itself as the only possibility of escape. Though tragically, as we all know, many depressed people do take their lives, for many even the will to take this action is not present. In bipolar disorder, the impairment of the motivating function of the will in depression mixes with the impairment of its restraining capacity in mania. One can neither move oneself in the desired direction nor restrain one’s thoughts and actions from running in every direction. The negative self-obsession of depression (which can still be justifiably considered delusional) alternates with (the often more noticeable to the outside observer) grandiose and exalted self-image and beliefs. Mania can either cycle back to depression or, through delusional tension, develop into acute psychosis.
The most characteristic symptoms of schizophrenia – hallucinations and elaborate delusions – are usually preceded by a prodrome which bears significant resemblance to certain aspects of depression and mania. This is often a period of social withdrawal, when the experience of the outside world seems to move from a sense of unreality to a sense of the profound yet ambiguous meaningfulness of all things. In healthy minds, identity provides a relatively stable image of the cultural world and the individual’s place in it, and thus the will directs thought and action towards relevant goals. Naturally, at each moment much of the environment is overlooked so that attention can be focused where it should be. In the prodrome, however, the thinking self becomes fixated on mundane aspects of reality, and things in the environment which are usually taken for granted become alternately senseless or imbued with special significance. This experience of the world as incomprehensible and inconsistent suggests a serious problem with identity. The will, (which in healthy cases is a largely unconscious process directed by identity), gets put on the shelf, so to speak, and the thinking self takes on the task of trying to piece together this unreal or hyperreal outside world.
The prodrome is usually only identified after the fact, since it is the appearance of hallucinations and delusions which allows the illness to be diagnosed as schizophrenia. Delusions, (often also present in patients diagnosed with bipolar), are the best known feature of schizophrenia. We can understand delusion as the inability to separate between subjective and objective realities, or put another way, the inability to distinguish between the cultural process on the individual level (the mind) and culture on the collective level. Thus internally-generated experiences are mistakenly thought to have originated outside. The elaborate delusions described by schizophrenic patients can be seen as a kind of rationalization of the experience of acute psychosis. It is important to distinguish between delusional accounts of the acutely psychotic phase, given after the fact in moments of relative self-possession, and the experience itself. In the midst of acute psychosis, a person is almost always incommunicative. Descriptions of this stage often mention the loss of the sense of self, as well as the sense of being watched by an external observer. The mental process, no longer individualized, is beyond willed control. Schneider’s first-rank symptoms, such as the belief that thoughts are extracted or implanted and that physical sensations and actions are controlled by an external force, clearly point to the experienced loss of will which runs underneath so many schizophrenic delusions. The sense of an alien presence is explained by the continued processing of the thinking self even after identity and will have (if only temporarily) disintegrated. Lacking this individualized direction, the “I of self-consciousness” becomes the “eye of unwilled self-consciousness,” – the defenseless sufferer necessarily experiences this free-ranging cultural process as foreign, and quite possibly terrifying, because it is beyond his control.
The formal abnormalities of thought which were so important to Eugen Bleuler’s diagnosis of schizophrenia also fit into the cultural framework. Schizophrenics are often unable to privilege conventional, socially-accepted associations in thought. Most of the time in our modern societies, normal associations follow the rules of logic, (in the strict sense of Aristotelian logic based on the principle of no contradiction). (However, it must be noted that logic is an historical, thus cultural phenomenon, so the inability to think logically should not be taken as evidence of brain malfunction). Of course, depending on the context, some other logic may be culturally appropriate, and arbitrating between contextual logics is one of the primary ways that the will directs thought. In schizophrenia, though, with the will impaired, thought is unanchored to any of these logics, and seems to jump from one to another at random. This becomes most evident in the use of language, which seems to speak itself, flowing without direction and often tied together by the sonic qualities of words or connections in meaning which would usually be overlooked as irrelevant. While the use of language will necessarily depend on the particular cultural resources present in the individual’s mind, it is impersonal in the sense that it draws it life from the associations inherent in language itself, rather than associations pertinent to individual identity or the objective cultural context.
Not only does Greenfeld’s continuum model better account for the huge overlap between the illnesses as currently defined, it also allows us to pay closer attention to movement along this continuum throughout the course of an individual’s illness. While anomie is presumed to be the initial cause of mental illness early in life through interference with identity formation, the various swings on the spectrum may become more comprehensible when we consider what is happening to the individual at the time when the change in symptoms occurs. It is possible that specifically anomic situations may lead to shifts in the already existing illness. (These considerations are explored in Greenfeld’s analyses of the well-publicized cases of John Nash, ( Nobel prize winner in economics), and Kay Redfield Jamison, co-author of the authoritative book on manic-depressive illness.)
The focus on the symbolic, mental processes at work in these “diseases of the will” should not be misunderstood as in any way taking away from the biological reality of major mental illness. Just as the activity of healthy minds corresponds to certain brain activity, so the abnormal processes of a sick mind would be expected to correspond to atypical patterns of brain function. Neither does the hypothesis that mental illness has a cultural rather than biological cause ignore potential genetic conditions that might make certain individuals more vulnerable than others. In fact, it is possible that mechanisms of interaction between culture and genes may become known with continued research in epigenetics – the study of changes in gene expression not caused by changes to the underlying DNA sequence. Some have already hypothesized that gene-environment interaction may lead to epigenetic changes that are central to the expression of mental illness. Of course, unless epigenetic research is specifically designed to take the symbolic nature of the environment into account, it will probably do little to help us to better understand mental disease and the mental process in general.
Part 1 of the exposition looks at the the mind/body problem which has stood at the center of Western Philosophy for over 2000 years, and considers Greenfeld’s proposed resolution – a 3 layer view of reality (matter, life, and culture/mind) in which the top 2 are emergent phenomenon. Greenfeld credits Charles Darwin with making it possible to view the world in terms of emergent phenomenon, which in turn makes possible her theory of culture and the mind which can put the mind/body question to rest. At the same time, she exposes the historical roots of the dogmatic bias of science (as it is normally practiced) towards materialism, and dismisses the notion that science has (or can) in any way empirically prove this position, thereby maintaining that there is no inherent conflict between faith and rigorous empirical study.
In part 2, the proposed solution to the dualist problem is developed – culture is a symbolic process emergent from biological phenomena and operating within the boundary conditions of life, yet fundamentally autonomous and governed by different set of rules. As life organizes the matter out of which it is composed into unlikely patterns, so the symbolic process of culture organizes the brain, (which at all times both supports and provides the boundary conditions for the process) to suit its own needs. Greenfeld logically deduces that the point of emergence for culture and the mind must have been the moment vocal signs were first intentionally articulated, and became symbols. The internalization of this intention creates the mental structure of the will. Yes, this means that in a single moment, culture, the mind, and “free will” as we know it appear together, forever separating homo sapiens from all other animal species and making humanity a reality of its own kind. This view of culture, as a symbolic process which not only structures social life but individual minds, has radical implications for the many disciplines which study the various aspects of humanity. This view also demands the attention of neuroscience, which will remain purely descriptive and not gain any ground in the attempt to understand and explain “consciousness” until it takes into account the symbolic reality – by far the most important aspect of the human environment.
Part 3 reiterates the ideas about nationalism developed in Greenfeld’s first two book and takes things a step further. She identifies nationalism, a fundamentally secular consciousness based on the principles of popular sovereignty and egalitarianism, as the defining element of modernity, responsible for massive changes in the nature of human experience. More specifically here, she claims that love, ambition, and madness as we know them today emerged out of this new consciousness in 16th century England and spread from there to other societies that adopted and adapted the nationalist culture.
Part 4 challenges the current psychiatric dogma that manic-depressive illness and schizophrenia are distinct illnesses with biological causes. The need to rethink this distinction is evidenced by the high degree of overlap in symptoms between two conditions and the failure to find consistent functional or structural brain abnormalities which would allow for accurate differential diagnosis. Not only have genetic researchers been unable to find individual genes that cause schizophrenia or mdi, their best work suggests a shared vulnerability to both illnesses. Epidemiological data seems to show that mental illness occurs at greater rates in modern nations with Western-derived culture, and studies within these nations suggest that the upper classes (i.e those individuals who fully experience the openness of society and have the greatest number of choices) are particularly affected. Both of these findings are consistent with Greenfeld’s hypothesis that anomie causes mental illness. Nevertheless, this data is consistently ignored or rejected as flawed, since it flies in the face of the currently accepted notion of mental illness as biologically caused and uniformly spread across cultures and throughout history. Likewise, the fact that no genetic cause of mdi or schizophrenia has been found has done little to dhake the faith that such a cause will one day be found. Unfortunately, this systemic materialist bias can only continue to impede progress in the understanding of these fatal conditions.
The theoretical view of mental illness as ultimately stemming from problems with the formation of identity is a new one, and thus it does not come packaged with some ingenious cure. However, the clear implication is that something must be done to help individuals in anomic modern societies to create well formed identities. Since this process begins very early in childhood, the intervention must begin then as well. Educating children about the multitude of choices they will face in their extremely open environment, and alerting them to the presence of the many competing and often contradictory cultural voices vying for their attention would become priorities. We should also be cautious (as the recent work of people like Ethan Watters suggests) of the potential side effects of exporting our culture to other societies.
While this exposition is in some sense finished, there is much more to say, and I will continue exploring these ideas and comparing them with other perspectives in my future posts. I realize this work is controversial, and can be difficult to take in all at once. Please, if any part (of the whole) of this seems unclear, unsupported, or simply outrageous, ask a question or give your critique. I’m eager to hear what others have to say.
Posted on October 1, 2010 - by David
I am working directly from the unpublished text of Liah Greenfeld’s forthcoming book, Mind, Madness, and Modernity: The Impact of Culture on Human Experience. All the original ideas, and all interpretations and analysis of primary and secondary source materials used to support the ideas are attributable to Liah Greenfeld. Read the introduction to the exposition here.
part 3 – Madness: A Modern Phenomenon
With all that has been written about schizophrenia and manic-depressive illness, the countless studies that have been conducted, and the growing list of medications used in treatment, it would be easy to mistakenly assume that we now understand the nature and cause of these ailments. The history of the separation of psychoses of unknown cause into these two categories leads us to Emil Kraepelin (1856-1926). This German psychiatrist believed that these were heritable brain diseases, and he led a revolution in classification in German-language psychiatry around the turn of the twentieth century, trying to discover just what kind of brain diseases he was dealing with. Kraepelin used a latin version (dementia praecox) of the French term demence precoce (coined in 1852 by Benedict Morel), to distinguish a form of insanity with an early onset and rapid development from the common geriatric dementia. Kraepelin then separated Dementia praecox from manic-depressive insanity (called by the French folie circulaire or folie a double forme). Up until that point, the two conditions were believed to constitute one general category of insanity.
Kraepelin’s use of the term dementia praecox, which suggested a progressive slowing of mental processes, to refer to a condition characterized largely by delusions and hallucinations, (which imply not mental lethargy but imaginative hyperactivity) may have contributed to the misinterpretation of schizophrenia, (still common today), as degeneration of cognitive/reasoning capacities. The evidence suggests that it is rather the strange character of thought, the inability to think in normal, commonly accepted ways, which distinguishes schizophrenia from geriatric dementia. The name “schizophrenia” (meaning “splitting of the mind”) was introduced to replace dementia praecox in 1908 by Swiss psychiatrist Eugen Bleuler. Bleuler saw the disease mainly in terms of four features: abnormal thought associations, autism (self-centeredness), affective abnormality, and ambivalence (inability to make decisions). Then in the 1930’s, another German psychiatrist, Kurt Schneider, contributed greatly to the diagnosis of schizophrenia by identifying “first-rank symptoms,” primarily related to hallucinations and delusions. Hearing voices speak one’s thoughts aloud, discuss one in the third person and describe one’s actions; feeling like an outside force is controlling one’s bodily sensations or actions and extracting, inserting, or stopping thoughts; believing that one’s thoughts are “broadcast” into the outside world – these are some of the experiences which Schneider found to be characteristic of the illness which Bleuler had recently renamed.
It should be noted that although Schneider’s first rank symptoms are essentially psychotic symptoms, (and schizophrenia is by definition a psychotic illness), very often those diagnosed with schizophrenia do not experience these symptoms. Diagnostic standards today distinguish between positive symptoms, (symptoms like hallucination and delusions which are not present in healthy individuals), and negative symptoms (e.g blunted affect, lack of fluent speech, inability to experience pleasure, lack of motivation). Anti-psychotic medications are often effective in treating some of the positive (i.e psychotic) symptoms of schizophrenia, but attempts to alleviate negative symptoms with medication have been largely unsuccessful, and the prognosis tends to be worse for sufferers who experience primarily negative symptoms.
By far the most authoritative and extensive work (over 1200 pages long) on that other half of madness is Manic Depressive Illness: Bipolar disorders and Recurrent Depression, written by Drs. Frederick Goodwin and Kay Redfield Jamison. The subtitle (Bipolar disorders and Recurrent Depression) added for the 2nd edition, (published in 2007), emphasizes the essential unity of all the major affective illnesses. In the introduction, the authors stress their reliance on Kraepelin’s model for their own conceptualization of mdi. (They, like Kraepelin, see it as a brain disease with genetics playing a significant causal role). But because Kraepelin’s major act of classification was to divide psychotic illness into two distinct disorders, any definition of mdi based on his work depends on having a clear definition of schizophrenia, which is clearly lacking. Kraepelin’s distinction between the two was based primarily not on differences in symptoms, but on course of illness and outcome, with schizophrenia (or in his terminology, dementia praecox) being much more malignant and causing significant deterioration over time. It was in fact Eugen Bleuler who first called mdi an “affective illness,” not because schizophrenia occurred without major mood disturbance, but because in mdi he saw it as “the predominant feature.” This characterization has proven to be extremely important for the current conception of major mental illness; the original distinction as between two psychotic illnesses has largely been obscured, and mdi is now viewed essentially as a mood disorder, with schizophrenia, by contrast, appearing to be essentially a thought disorder.
Though manic-depressive illness includes a variety of mood disorder diagnoses, the main distinction is between major depression and bipolar disorder (alternating episodes of depression and mania). A few decades ago, the bipolar label was split into bipolar-I and bipolar-II. Bipolar-I is the severe form of the disease in which both depressive and manic episodes are serious enough to require treatment. A diagnosis of bipolar-II may be given when a patient suffers from major depressive episodes and also experiences “hypomanic” episodes (meaning basically “mildly manic” and therefore lacking psychotic features). Even Goodwin and Jamison seem skeptical of the value of this and other divisions in classification.
In order to compare manic-depressive illness with schizophrenia, then, we should concentrate on descriptions of, (go figure), depression and mania. According to the DSM-IV, typical symptoms of depression include “loss of interest or pleasure in nearly all activity,” irritability, “changes in appetite and weight, sleep, and psychomotor activity; decreased energy; feelings of worthlessness or guilt; difficulty thinking, concentrating, or making decisions; [and] recurrent thoughts of death or suicidal ideation, plans, or attempts.” The description given by Goodwin and Jamison is along the same lines, though much more vivid:
Mood in all of the depressive states is bleak, pessimistic, and despairing. A deep sense of futility is often accompanied, if not preceded, by the belief that the ability to experience pleasure is permanently gone. The physical and mental worlds are experienced as monochromatic, as shades of gray and black. Heightened irritability, anger, paranoia, emotional turbulence, and anxiety are common. (MDI 66)
Further descriptions from patients and clinical observers add more layers to this general body of symptoms; among the most interesting, lack of facial expression, and a sometimes frightening sense of unreality. It is quite clear that depression is something altogether different from normal sadness, and even “abnormally low mood.” These descriptions show a huge variation in the level of emotion experienced, from almost no feeling at all, to unbearably acute anxiety. A depressed person’s thinking may be slowed almost to the point of paralysis, or he may alternately be unable to control an unending torrent of painful thoughts. All that seems consistent within descriptions and definitions of depressive episodes is that it is an extremely unpleasant experience.
There is such a diagnosis as psychotic depression, (featuring obvious delusions and hallucinations, in which case it is not clear how it can be diagnosed differently from schizophrenia) but even its more ordinary form, many of the symptoms of depression cannot be easily distinguished from the negative symptoms of schizophrenia, which include flat affect and paralyzed thought. And what good reason is there not to consider the firm belief in one’s utter worthlessness, the obsession with death, and the sense of the absolute necessity of ending one’s life as instances of delusion or thought disorder?
Just as depression is not just extreme sadness, mania is not an exaggerated form of joy. According to the DSM-IV, a manic episode is a period of “abnormally and persistently elevated, expansive, or irritable mood,” with typical symptoms being “inflated self-esteem or grandiosity, decreased need for sleep, pressure of speech, flight of ideas, distractability, increased involvement in goal-directed activities or psychomotor agitation, and excessive involvement in pleasurable activities with a high potential for painful consequences.” To be considered a manic (rather than merely “hypomanic) episode, “the disturbance must be sufficiently severe to cause marked impairment in social or occupational functioning or to require hospitalization or it is characterized by the presence of psychotic features.” Mood within a manic episode may be highly variable, and the frequent alternation between euphoria and irritability is noted.
Grandiose delusions are common – the extreme expression of the inflated sense of self-importance so typical in mania. (Again, one wonders why the beliefs which spring from the typical sense of worthlessness in depression – the polar opposite of the grandiose beliefs in mania – should not be considered delusions as well). Grandiosity often manifests in compulsive writing which the sufferer may believe has special significance but is usually characterized by “flight of ideas” and “distractability.” This behavior is not unique to mania, and has been well documented in patients diagnosed with schizophrenia.
Delusions may be not only grandiose, but, (as in schizophrenia), paranoid as well. In some severe cases, the sufferer may reach the stage of delirious mania, which the authors of MDI describe by quoting Kraepelin:
At the beginning the patients frequently display the signs of senseless raving mania, dance about, perform peculiar movements, shake their head, throw the bedclothes pell-mell, are destructive, pass their motions under them, smear everything, make impulsive attempts at suicide, take off their clothes. A patient was found completely naked in a public park. Another ran half-clothed into the corridor and then into the street, in one hand a revolver in the other a crucifix….Their linguistic utterances alternate between inarticulate sounds, praying, abusing, entreating, stammering, disconnected talk, in which clang-associations, senseless rhyming, diversion by external impressions, persistence of individual phrases are recognized. …Waxy flexibility, echolalia, or echopraxis can be demonstrated frequently. (36)
The descriptions of delirious mania provided by recent clinicians are similar to Kraepelin’s. Quite obviously, a patient in the condition described above is suffering from some of the most characteristic symptoms of schizophrenia. Of course for those following in Kraepelin’s footsteps, this similarity should come as no surprise, since (as was mentioned earlier) his distinction between the two psychotic disorders was not based on differences in symptoms. Indeed, the need to clarify the blurry boundary between psychotic mania and schizophrenia has resulted not in further distinction, but the creation of hybrid diagnostic categories like schizoaffective and schizo bipolar. In summarizing the findings of a number of studies over a thirty year span comparing thought disorder in schizophrenia and mania, Goodwin and Jamison are forced to conclude that there is no quantitative difference in thought disorder between the two conditions. Nevertheless, (needing to maintain the distinction between their area of expertise and the even more mysterious realm of schizophrenia) they maintain there are qualitative differences in thought disorder, though the studies used to support this claim point in a number of different directions. Of course, these studies were done only after patients received a particular diagnosis, so differences in thought disorder may also have been related to the effects of different medications. After considering the huge overlap between these two diagnoses, and the fact that differences seem to be more of degree than kind, it seems possible that perhaps they might not be two distinct diseases after all.
While the technological advancements of recent decades allow us to map the human genome and look at the brain on the molecular level, the enormous amount of data that has been amassed is virtually useless for psychiatrists trying to diagnose their sick patients because the assumed biological causes of schizophrenia and manic-depressive illness have not been found. No brain abnormalities that are specific to either illness or present in all cases have been identified. Nevertheless, the experts who study and treat schizophrenia and mdi keep the faith (quite literally) that a breakthrough is just around the corner.
For years, genetic research has appeared to be the most promising of the recently opened avenues, but the excitement seems unwarranted by the findings. The relatively large number of chromosomal regions which may be implicated in susceptibility for bipolar means that hope of finding a specific bipolar gene or even a small number of genes must be given up. Some researchers think the way to go is to narrow the search by looking for genes associated with specific aspects of the disease. Of course, this further refinement is only possible because of the huge variation in symptoms and experiences of those who fall under the mdi/bipolar umbrella, and we are once again reminded of the difficulty of defining what this illness or group of illnesses even is. Furthermore, even the distinction between schizophrenia and mdi seems to collapse in light of the genetic linkage data. Goodwin and Jamison write:
While the search for predisposing genes had traditionally tended to proceed under the assumption that schizophrenia and bipolar disorder are separate disease entities with different underlying etiologies, emerging findings from many fields of psychiatric research do not fit well with this model. Most notably, the pattern of findings emerging from genetic studies shows increasing evidence for an overlap in genetic susceptibility across the traditional classification categories. (49)
Genetic studies in the schizophrenia research community lead to pretty much the same hypothesis as with bipolar: genetic susceptibility is most likely polygenic, meaning dependent on the total number of certain genes which may contribute to vulnerability. It must be noted that genetic vulnerability is a condition, not a cause of schizophrenia and bipolar – something else must be acting on this vulnerability. In one way or another, this fact is usually noted in the literature that deals with genetic data, but it is often obscured by a tone of confidence which suggests the information may be more meaningful and explanatory than it truly is.
Even when a specific gene has been well studied across illnesses, its usefulness in understanding genetic susceptibility may be extremely limited. Some studies in both schizophrenia and mdi have found an increased risk of illness for those who possess the short form of the serotonin transporter promoter gene 5-HTT. The thing is, each of us has two copies of this gene, and over two-thirds of us have one long and one short form, meaning that having the normal variant of the gene is the risk factor! If most of us possess a gene which puts us at risk for an illness which only a small minority of people have, then this particular trait is obviously not much of a causal explanation.
Still today, the most important evidence for the heritability of schizophrenia and bipolar are traditional genetic-epidemiological studies – “genetic” research only in the sense that we know that relatives share genes. There is significantly greater lifetime risk of illness for people with a first degree relative who suffers schizophrenia, and studies of bipolar and major depression (i.e manic-depressive illness) have had parallel findings. However, the overwhelming majority of schizophrenics do not have parents or first-degree relatives with schizophrenia, and most of them do not have children themselves, making it difficult to establish the genetic component by looking at family history in a large percentage of cases.
Studies of twins are particularly important for the heritability argument. Calculations from these studies find a 63% risk of having bipolar disorder if an identical (monozygotic) twin has it. The risk for major depression is significantly lower. In schizophrenia the risk is under 50%. The ideal study design for attempting to separate the contributions of biology and environment involves identical twins, separated at birth, adopted, and raised apart, with at least one of them suffering from mental illness. As can be imagined, these cases are hard to come by (4 in mdi and 14 in schizophrenia), and the small number of cases makes generalization suspect (though generalizations are often still made). Another method, for which there is significantly more data, is to compare the risks of identical (monozygotic) and fraternal (dizygotic) twins. Because both kinds of twins are assumed to share the same environment, but fraternal twins only share 50% of their genes, the difference in risk between fraternal and identical twins is attributed to genetics. But this method depends on an extremely limited understanding of environment, reducing it to simply having the same parents. It’s likely that identical twins would be treated in very similar ways by their parents and society at large, but fraternal twins, being biologically different (perhaps even in gender) will likely be treated in very different ways. Therefore, it is highly doubtful that twin studies are able to separate the contributions of biology and environment to lifetime risk of mental illness to anywhere near the degree that is suggested. The fact that over one-third of identical twins are not affected by the disease from which their twin suffers reveals again that genetic susceptibility is at most a condition, and not a cause of schizophrenia and mdi.
The prevailing assumption that schizophrenia and mdi have biological causes naturally leads to the expectation of finding them distributed uniformly across cultures and throughout history. In the case of schizophrenia, this belief justifies the adoption of the standard worldwide lifetime risk of 1%, (a nice round number), extrapolated from an embarrassingly small number of studies – one from Germany in 1928, and two from the 1940’s in rural Scandinavian communities. However, there is a serious lack of evidence of the existence of these illnesses before the early modern period, and studies have consistently found significant differences in the rates of mental illness across cultures and between social classes within cultures. Nevertheless, (perhaps because the idea that serious mental illness may affect different populations at different rates does not sit well with us), variations are often explained away with charges of inaccurate reporting and under or over diagnosis. But epidemiological studies sponsored by the World Health Organization carried out over several decades have found that the illness identified as schizophrenia in poorer, “developing” countries tends to be less chronic (fewer psychotic episodes), causes less disability, and has a better prognosis than schizophrenia in more affluent, “developed” societies. Some of the data from Western nations suggests a lifetime risk of schizophrenia greater than 1%, while in poorer societies the number often appears lower. Multiple studies have found the rate of schizophrenia among Afro-Carribeans born in the UK to be higher than the prevalence in the islands from which their families immigrated. Both schizophrenia and mdi have been found to be less prevalent in Asian countries.
Overall, cross-cultural data supports the hypothesis that schizophrenia and mdi are diseases caused by modern culture, and more specifically, that the more anomic a society becomes, (i.e the more identity becomes a matter of individual choice and the less guidance is given by culture), the more mental illness will be found. Research in the U.S has shown a lower age of onset and higher rates of prevalence for manic-depressive illness in those born after 1944 compared to those born before, though this increase has been attributed to the inadequacy of earlier data-collection techniques, which systematically underestimated the true prevalence of affective disorders. Usually, when environment is allowed a causal role in mental illness, poverty and the stress of the urban environment is the safest target to blame, with studies as early as 1939 finding a higher incidence of schizophrenia in lower-class, urban areas. However, when studies began to consider social class of origin rather than merely the status of the patient when the illness was first recognized, the picture changed significantly. The social mobility of schizophrenic patients displays a “downward drift,” suggesting that their greater proportion among the lower class is due to the disability of the disease rather than the stress of this environment. Furthermore, it appears that the upper-class supplies more schizophrenics than could be predicted by the total upper-class share in the population. The majority of studies of manic-depressive illness show significantly lower rates in blacks compared to whites, but this, like so many other findings which make no sense within the biological framework, is dismissed for a variety of reasons as a mistake.
Finally, Goodwin and Jamison tell us that “the majority of studies report an association between manic-depressive illness and one or more measures reflecting upper social class.” (169) To explain this finding, they consider the possibility that certain personality traits associated with affective illness may contribute to a rise in social position. (One assumes they mean the occasionally “positive” aspects of mild mania, since it is unclear how crippling depression or delusional mania would aid in social climbing). A second hypothesis, that manic-depressive illness could be related to the particular “stresses of being in or moving into the upper social classes,” is deemed simply “implausible, because it assumes that, compared with lower classes, there is a special kind of stress associated with being in the upper social classes, one capable of precipitating major psychotic episodes.” Furthermore, they accuse such a hypothesis of ignoring genetic factors, though discounting genetic vulnerability as a condition for mdi is quite obviously not implied by this idea.
By now it should be quite clear that the belief that major mental illness is caused biologically has made it virtually impossible to reconsider what the empirical evidence actually tells us. Each time the research that is supposed to support this belief comes up short, it is another occasion for the reaffirmation of faith in a soon-to-come breakthrough. Where the data appears to blatantly contradict their hypothesis, they often simply discount its reliability. While many of the most important experts will freely admit how little we actually understand about mental illness, despite all efforts, it is hard to imagine the direction of these efforts will change much anytime soon. This is not a recipe for scientific progress.
The final post of this series will bring Greenfeld’s theory of the mind together with what we know about schizophrenia and manic-depressive illness, considering the two as one disease existing on a continuum of complexity of will-impairment.
Posted on March 17, 2010 - by David
The authors of a study recently published in the journal Biological Psychiatry claim that influenza infection during pregnancy may play a role in the development of schizophrenia later in life.
According to the abstract, twelve pregnant rhesus monkeys were infected with influenza early in the third trimester, and 7 healthy subjects were used as a control group. The brains of the babies were scanned using MRI after one year, and the researchers found that “exposed offspring had significantly smaller cingulate and parietal cortical gray matter and left parietal white matter than nonexposed offspring. Bilaterally, cingulate white matter was greater in exposed offspring than in controls.” (Gellner, Journal Watch Psychiatry) It is this finding that gets translated into a sentence like “The results showed ‘a significant effect’ which mirrored brain changes in schizophrenic humans” which I read in a short news clip on the Dallas-Fort Worth Fox News affiliate website, under the (only slightly misleading) title ‘Scientists Find Link Between Pregnant Women with Flu and Schizophrenia.’
The study’s main author, Sarah Short, chose her words a little more carefully:
“This was a relatively mild flu infection, but it had a significant effect on the brains of the babies,” Short said. “While these results aren’t directly applicable to humans, I do think they reinforce the idea, as recommended by the Centers for Disease Control and Prevention, that pregnant women should get flu shots, before they get sick.”
But obviously, the object of the study wasn’t merely to reinforce the idea that pregnant women should get flu shots. The hypothesis that flu infection during pregnancy might play a role in the development in schizophrenia was first put forth over 20 years ago, in a study involving a Finnish cohort born during the 1957 influenza pandemic. They found that “those exposed to the viral epidemic during their second trimester of fetal development were at elevated risk of being admitted to a psychiatric hospital with a diagnosis of schizophrenia,” but the results of similar studies have varied considerably. To date, only about half of the 25 research papers examining this phenomenon have confirmed these findings. Those who support this hypothesis often cite one of the more recent and “scientific” studies, which looked at maternal blood tests to confirm when and if those diagnosed with schizophrenia were exposed to the flu. The 2004 investigation found that “the risk of schizophrenia was increased 7-fold for influenza exposure during the first trimester.” If this is indeed true, it’s easy to understand why the authors considered it significant, but the finding that “there was no increased risk of schizophrenia with influenza during the second or third trimester,” conflicts with the earlier studies which claimed that risk of schizophrenia was increased with second trimester exposure. Based on the available data, it’s impossible to draw any conclusions about the relationship between schizophrenia and prenatal exposure to the flu, but obviously, as the recent publication of the monkey study demonstrates, researchers are still actively pursuing this track.
A few questions/criticisms about this study from someone with an admittedly (very) limited knowledge of neurology…
Is there a difference between contracting the flu virus in the typical way and forced infection, in terms of effects on the fetus?
If the available data points to first or second trimester exposure as a risk factor, what is the comparative value of this study considering the pregnant monkeys were infected during the third trimester?
What are other health effects for children of mothers who have the flu while pregnant? Has there been any research examining the relationship between prenatal exposure to influenza and any other mental illnesses?
If this really is a significant risk factor, wouldn’t it suggest that in developing countries where the flu vaccine is less readily available, there should be higher rates of schizophrenia?
A summary of the study by Asian News International (available on many websites) says that “rhesus monkey babies born to mothers who had the flu while pregnant had smaller brains and showed other brain changes similar to those observed in human patients with schizophrenia.” To my knowledge, schizophrenics do not have “smaller brains,” and from what I’ve read, nearly every region of the brain and every neurotransmitter has been implicated by one study or another in the etiology or progression of schizophrenia. It seems a bit misleading then to represent the changes observed in the monkey’s brains as “similar to those observed in human patients with schizophrenia.” This may be the fault of the news article and not the study authors, but I feel it’s important to point out that despite all our technology and the proliferation of research into the “biological basis” of schizophrenia, there is no test or scan, no specific brain changes that can be identified and used to diagnose schizophrenia.
Because so many potential genetic and neurological risk factors are being investigated and written about, there can be a false sense that we are approaching an understanding of what causes schizophrenia. But risk and vulnerability are merely that: factors which increase the possibility that a person exposed to the cause of schizophrenia will go on to develop the disease. In the first chapter of a 2007 book called Recovery from Schizophrenia, Norman Sartorius, former President of the World Psychiatric Association and former Director of the World Health Organization’s Division of Mental Health, writes:
“Despite advances in our knowledge about schizophrenia in the past few decades, nothing allows us to surmise that the causes of schizophrenia will soon become known, or that the prevention of the disorder will become possible in the immediate future.” (3)
Sure, I like monkeys, and I understand how biologically similar we are, but if we want to understand schizophrenia, perhaps we should be looking in the realm of what makes us human.
Posted on February 22, 2010 - by David
I regret how spotty my posts have been lately, but if I’m not writing something new every day the best thing I can do is point you to someone else’s work. With the proposed changes for the DSM-V being made public last week, there are plenty of opinions floating around on the internet. I found this op-ed piece from the Wall Street Journal by Yale psychiatrist Dr. Sally Satel interesting.
She points out that many of the proposed changes, (as well as the opposition to those changes), have more to do with stigma, labels, and identity issues than actual advances in the understanding of mental illness. Satel also mentions the common overlap in symptoms and diagnoses within individual patients, and underlines our relative ignorance as to how genes are actually related to mental illness:
The other problem that confounds psychiatry is how to draw boundaries around diagnostic categories, given that we rarely know the cause of mental illness at the neural level. Mental illnesses are the product of numerous genes that interact with one another, with the environment and also with experience. (A recent study by the National Institute of Mental Health found that 80 genes could be associated with bipolar disorder.) Add to this the miasma of social and personal encounters that impinge upon the genetically vulnerable individual—stress, poverty, family instability, drug or alcohol use, and so forth—and the causal mechanisms of any mental illness become staggeringly complex and elusive. Moreover, the “psychopathological pie,” as a colleague calls it, is rarely divided up as tidily as the manual implies. Patients often have symptoms that sprawl across several diagnostic categories. For example, half of kids who receive the diagnosis of bipolar disorder also have ADHD.
Of course, if you’ve been a regular reader of this blog you won’t be surprised that I take slight issue with her explanation of mental illness, (even though it might not be totally fair to judge her based on one sentence in a WSJ op-ed piece). The inadequacy of her own definition is made clear when she mentions that “80 genes could be associated with bipolar disorder,” but says nothing about how these genes “interact with each other.” Also, what is meant by “environment” and “experience” is unclear and could be taken in a variety of ways. She seems to offer a broad explanation for mental illness and demonstrates well that there major issues with the way we classify symptoms as disorders which often overlap, but like a good psychiatrists she still locates cause with genetics or “at the neural level.”
MindHacks has an extensive summary of the DSM-V changes with links to other major media coverage. I found his comments on the restructuring of the schizophrenia diagnosis and the addition of ‘psychosis risk syndrome’ particularly interesting. His article suggests that a lot of the more subtle changes are aimed at “de-freuding” the DSM. Definitely worth your time to check this out.
Posted on February 17, 2010 - by David
At the close of a 20 year long study, researchers from the University Hospital of Copenhagen claim that “children of mothers who had been diagnosed with anemia during pregnancy, most likely due to iron deficiency, had a significantly elevated risk of developing the mental disorder. ” You can check out the article where I first read about the findings, or look at an abstract of the research paper, published in the Schizophrenia Bulletin.
Once again, I find myself less than impressed with the analysis of the data gathered and the conclusions drawn. I quote the Reuters news article:
To further investigate this potential link, Srensen and colleagues analyzed the psychiatric outcomes of a large group of Danish children born between 1978 and 1998 — the biggest cohort in which the relationship has been examined. Each child was followed from age 10 until the onset of schizophrenia, death or the study’s closure on December 31, 2008.
Among 1,115,752 newborns, 17,940 (1.6 percent) were exposed to anemia in the womb. A total of 3,422 — including 41 from the exposed group — went on to develop schizophrenia, according to the report published in the journal Schizophrenia Bulletin.
After accounting for differences between the two groups and other relevant factors, including the parents’ ages and history of mental illness, exposure to anemia in the womb was associated with a 60 percent increased risk of schizophrenia in offspring during the 20 years of the study.
The researchers further concluded that 0.58 percent of schizophrenia cases (a total of about 20 diagnoses) could have been prevented had there been no cases of anemia among the mothers.
Now I don’t claim to be a statistician. I took two semesters of stat in college to fulfill my math requirement, and let’s just say my attendance wasn’t great. Still, I can’t seem to resist doing some of my own number crunching…
- 41 schizophrenics in the exposed group / 17,940 exposed to anemia = a prevalence rate for schizophrenia of approximately 0.2% for those exposed to anemia in the womb
- 3,422 total cases of schizophrenia – 41 exposed cases= 3381 schizophrenics not exposed
- 1,115,752 total children – 17,940 children exposed to anemia = 1,097,812 children not exposed
- 3381 / 1,097,812 = a prevalence rate for schizophrenia of approximately 0.3% for those not exposed to anemia in the womb
Obviously, 0.3% is greater than 0.2%, but after adjusting for potentially confounding factors, the researchers still arrive at the conclusion that “exposure to anemia in the womb was associated with a 60 percent increased risk of schizophrenia in offspring.” According to my best reading, this adjustment leaves them with only 20 cases of schizophrenia among those exposed to anemia which could not be attributed to some other factor. If the adjustments cut the number of the exposed cases in half, and they still determine that this group has a 60% greater risk of developing schizophrenia, then obviously the total number of schizophrenic cases they are working with has also been drastically reduced. It seems pretty bold to make this claim about increased risk on the basis of 20 cases, but my lack of statistical expertise probably renders me unqualified to make this judgment. Still, the simple fact that adjustment for confounding factors dramatically altered the size of the group is a little reminder of how many and how varied are the explanations for the cause of schizophrenia. Even if it’s true that about one half of one percent of all cases of schizophrenia can be attributed to iron deficiency anemia, does this really get us any closer to understanding the origins of this destructive mental illness?
A few last thoughts. According to my admittedly brief google research conducted this afternoon, iron deficiency is probably the most common nutritional deficit in the world, and I would assume that iron deficiency, (and therefore iron deficiency anemia), is more common in less developed parts of the world. So, if Iron Deficiency Anemia during pregnancy is a significant cause or contributor to the development of schizophrenia, then why aren’t the rates of schizophrenia higher in less developed countries? This line of reasoning would also suggest that rates of schizophrenia should have been higher centuries ago when diets were poorer and fewer resources were available, but it appears that this is not the case.
Posted on February 2, 2010 - by David
This article summarizes the results of a study from the University of Melbourne, which suggests that the omega-3 fatty acids found in fish oil may help prevent psychosis in adolescents and young adults who have been identified as “at-risk.”
The study involved 81 individuals ages 13-25 “who met at least one of the following three criteria: having low-level psychotic symptoms; having transient psychotic symptoms; or having a schizophrenia-like personality disorder or a close relative with schizophrenia, along with a sharp decline in mental function within the past year.”
For 12 weeks, half the group was given fish oil capsules and the other half recieved placebo. Participants were then monitored for next 40 weeks. Only 2 of the 41 people given fish oil developed a psychotic disorder compared to 11 of 40 of the placebo group. The omega-3 group also “also showed significant reductions in their psychotic symptoms and improvements in function.” The researchers hope to replicate the findings in a multicenter trial involving 320 people.
Certainly, the lack of adverse side effects compared to the commonly used anti-psychotic medications would make this treatment a much preferred choice for patients. While these findings are definitely positive, it was a very small and relatively short-term study, so further research is obviously needed to determine the value of fish oil as a treatment or preventitive measure for serious mental illness. Also, this once again highlights how little is understood about what is happening in the brain of the schizophrenic patient. The article mentions some of the potential reasons this novel treatment may be effective:
There are a number of mechanisms through which omega-3s could protect the brain, Amminger said; they are a major component of brain cells. They are also key to the proper function of two brain chemical signaling systems, dopamine and serotonin, which have been implicated in schizophrenia. Fish oil also boosts levels of glutathione, an antioxidant that protects the brain against oxidative stress.
In the quest to understand the cause and progression of this illness, nearly every neurotransmitter and every part of the brain has been implicated in some way or another. While hopefully this study will lead to new ways of dealing with the symptoms of schizophrenia without the devastating side-effects of many commonly prescribed drugs, it seems to be another example of a “scientific” answer which amounts to, “this might work, and if it does, these might be some of the reasons why.”
Posted on January 24, 2010 - by David
Chapter 3- The Shifting Mask of Schizophrenia in Zanzibar
In the first two chapters of Ethan Watters’ new book, Crazy Like Us: The Globalization of the American Psyche, we encounter the idea that differences in source of identity and social integration between cultures may account for differences in the expression, (and prevalence), of mental illness. The third chapter suggests that cultural differences may also explain the rather enigmatic finding that those diagnosed with schizophrenia in the “developing” world seem to fare better than their Western counterparts. I found anthropologist Juli McGruder’s case studies particularly interesting, as they raise the possibility that the cause, or at least trigger, for schizophrenia may lie in cultural conditions.
I think it’s worth noting, as Watters points out, that despite the privileged position science has been given in the study of schizophrenia and all the technological advances of the last few decades, we still know very little about the causes of this strange affliction.
More than any other mental illness in the Western world, this one belonged to the “hard scientists” who looked for the causes in bad genes, biochemistry, and the structure of the brain. The advent of brain scans – allowing a researcher to see into the head of live patients – brought with it a seemingly endless series of theories about the root cause of the illness. Abnormalities supposedly key to schizophrenia have been reported in the frontal cortex, the prefrontal cortex, the basal ganglia, the hippocampus, the thalamus, the cerebellum – and pretty much every other corner of the brain as well. No firm consensus had emerged about the location or cause, but there was wide agreement that the exciting advances in understanding the disease were coming from the laboratories of brain researchers.(134)
In the meantime, there are others like Juli McGruder who, (like sociologist Liah Greenfeld), believes that “culture and social setting play a more complicated role in the disease than simply influencing the content of the delusions.” (136) Scholars on the cultural side of the fence point to the results of two international studies by the World Health Organization. The WHO research, which began in the 1960’s and lasted 25 years, suggests that the severity of schizophrenia is not the same worldwide. Watters summarizes the findings:
What they found was that those diagnosed with schizophrenia living in India, Nigeria, and Colombia often experienced a less severe form of the disease (had longer periods of remission and higher levels of social functioning) than those living in the United States, Denmark, or Taiwan. Whereas over 40 percent of schizophrenics in industrialized nations were judged to be “severely impaired,” only 24 percent of patients in the poorer countries ended up similarly disabled. (137)
Liah Greenfeld believes that anomie, which she considers a built-in feature of modern culture, causes problems with identity formation which often lead to mental illness. In Nationalism and the Mind, she describes this phenomenon and its effects on individuals:
Anomie, commonly translated as “normlessness,” refers to a condition of cultural insufficiency, a systemic problem which reflects inconsistency, or lack of coordination, between various institutional structures, as a result of which they are likely to send contradictory messages to individuals within them. On the psychological level anomie produces a sense of disorientation, of uncertainty as to one’s place in society, and therefore as to one’s identity: of what one is expected to do under the circumstances of one sort or another, of the limits to one’s possible achievement… (14)
The chronic, modern state of anomie may not (yet) be a built-in a feature of Zanzibari culture, but when we use the word “developing” to describe a country or culture, we imply that they are developing into something more like us, i.e moving towards modernity. This process of modernization is necessarily anomic:
Anomie, is, in fact, the ultimate cause of cultural change. It both breaks the old cultural routine and encourages the formation of a new one. The general pattern of human history can be imagined as an alteration between relatively brief and rare periods of widespread (though culturally localized) anomie and cultural routine. Widespread anomie, most commonly implying gross inconsistencies between elements of culture impinging on individual identities, specifically inconsistencies within the system of social stratification which defines a person’s position in the social world in general and vis-à-vis particular others, affects large groups of individuals and expresses itself in social turmoil. (14-15)
I wasn’t surprised, then, to see the title ‘Revolution and Madness’ above the section introducing McGruder’s first case study. Watters describes the state of affairs in the country at the time when Hemed began to experience symptoms of schizophrenia:
After years of being a British colony, Zanzibar embarked on the uncertain path to self-governance. There were three political parties, twenty-two trade unions, and sixteen partisan newspapers stirring up anger and resentment on all sides. Hemed’s first experience of derangement, McGruder believes, was sparked by the social upheaval of the time. (142)
Given what was going on in that moment in the history of Zanzibar, the amount of stress felt by Hemed must have been intense. He was a middle-class man from a high-profile Arab minority at a time of growing racial and class distrust. His curly dark hair and facial features made him identifiably Arab. There seemed to be no safe political refuge. Even the political party he belonged to, the Zanzibar Nationalist Party, was internally split between those who considered themselves African and those of Arab heritage. No one knew whom to trust. (143)
We can also see how conflicting cultural messages may have played a role in the experience of Kimwana, Hemed’s daughter who suffered from the same illness.
She was a happy child even though her early years were turbulent times for the island. Her mother and classmates remember her as the brightest student in the class. Particularly skilled with numbers, she graduated from secondary school and took a job with the Ministry of Finance. This was 1983, a time of rapid change for women on the island. To fill in for the many educated men who had fled the political upheaval, women were beginning to enter the professional workforce by the thousands. (144)
While we in the West would see these new opportunities for women aa a change for the better, there still existed traditional guidelines on behavior which seemed to contradict this elevation in social status. It was only a few months after Kimwana started her new job that she began to hear male voices “gossiping that she was a disloyal and disrespectful daughter and sister” (146). Before the cultural changes which led to an influx of women into the workplace, Kimwana’s identity would have been based primarily on her relationship to her family and in behaving according to the prescriptions of the Islamic religion.
Much of the torment of having these male presences in her head related to Islamic rules of female modesty. While the voices were with her, she felt she must respect the codes of conduct as is she were actually in the presence of a man. At such times she could not bathe or undress and she tried not to go to the bathroom. Although she sometimes found it helpful to argue with the voices when they became critical, her sense of decorum made it difficult to do this out loud. (146-147)
In this section of the chapter, Watters highlights McGruder’s amazement at the ability of Amina, the mother and effectively the head of the household, to care for the large family and its two sick members. Her daily activities seem to far surpass western notions of busyness, and she takes the extra load created by mental illness in stride. This is possible, I believe, because she is secure in her identity in a way that neither Hemed nor her daughter Kimwana could be. She was raised to serve her family and God, and that is what she does. McGruder compares the Western, Christian attitude towards adversity to Amina’s stance and sees an importance difference.
In the cosmology of Western Christians, life’s challenges provide opportunities to become stronger and to have a closer relationship with God. The burdens God sends to Christians in the Western world are incitements to self-improvement. The comforts that Amina found in her religious belief, by contrast, were not in an encouragement to overcome or learn from hardships. Rather, simply accepting her burden was a continuous act of penance. (155)
In other words, the challenge of caring for her sick relatives did not provide a reason to change her identity. Her identity was essentially unchanged since childhood, she was merely to continue behaving and believing as she always knew she should. Unfortunately for her daughter, the conflict between the new cultural value of work for women, and the traditional emphasis on family and religion proved too much for her mind to handle.
The chapter also describes the damage often done by family members’ emotional over-involvement in the lives of their schizophrenic loved ones. This cultural tendency, according to Watters, is closely related to the Western emphasis on individual identity and the belief that individuals should be able to control their own destinies. As in the previous two chapters, the resounding message is that the highly individualistic nature of identity in modern societies and the lack of clear, shared cultural beliefs and practices lead to more widespread and more severe forms of mental illness.