Posts Tagged ‘bipolar’
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I am working directly from the unpublished text of Liah Greenfeld’s forthcoming book, Mind, Madness, and Modernity: The Impact of Culture on Human Experience.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 February 12, 2010 - by David
According to an article I read on Wednesday, a new diagnostic category is expected to be included in the upcoming DSM-V which may provide psychiatrists with an alternative to diagnosing the most troubled kids they see with bipolar disorder. The creation of the new diagnosis, called temper dysregulation disorder with dysphoria, seems aimed at dealing with concerns over the growing prevalence of the lifelong, stigmatizing bipolar label among children.
Back in the 90’s, thanks largely to the work of one Dr. Janet Wozniak, an assistant professor of psychiatry at Harvard, the bipolar diagnosis was stripped of one of its most defining characteristics as professionals puzzled over what to do with children with ADHD who were prone to particularly persistent and disruptive outbursts. The traditional definition of bipolar was closely tied to the presence of alternating periods of mania and depression, but these kids rarely if ever experienced the typical episodic fluctuations. In order to make the new use of the diagnosis stick, some argued that in children, the episodes might be very brief and occur many times throughout the day. Critics of the extended application complained that “there wasn’t good evidence that these kids grew up to be bipolar, and that if you looked backward at bipolar adults, they didn’t necessarily have these uncontrolled anger issues when they were young.” Nevertheless, the pediatric bipolar diagnosis quickly spread, and Wozniak maintains this is “because it made clinical sense.”
The article suggests that part of the shift to childhood bipolar diagnoses may have been related to a desire to treat this kind of behavior as a disease which could be dealt with via medicine. The only other diagnostic option seemed to be conduct disorder, which usually wasn’t treated with medication and seemed to imply a parental failure. Now, with TDD, the behavioral and mood problems can still considered a medical illness, but those diagnosed aren’t necessarily lumped into a category of people required to take drugs for the rest of their lives.
What really struck me when reading this article was how the language used to talk about this stuff makes it so plainly obvious that these psychiatrists and researchers really don’t know what it is they are dealing with. First of all, the shift in diagnosis in the 90’s had nothing to do with any breakthrough discovery about how the brains of children with behavior problems function. Basically, the symptom-based definition of a particular mental illness was revised or expanded to fit the troubling phenomenon that psychiatrists were observing. That is not how science is supposed to be done. To quote the article: “research psychiatrists worried that the children were being given a label that wasn’t right for them, and saddled with the sentence of a serious mental illness for the rest of their lives.” A label? Is it an illness, or just a label? Does the naming of the thing determine its nature? And if people have a serious illness of any kind, doesn’t it exist independently of any “sentence”?
I find it strange that the word ‘label’ is used over and over again and there’s all this talk about categories or diagnoses being created and changed in order to deal with stigma and avoid offending parents, and yet these psychiatrists believe that whatever it is they are talking about is unquestionably a problem with the brain. I mean, isn’t the reason they can’t decide what to call it that they can’t pin down what is actually happening with these kids? I can’t help but shake my head when I read that “it will be seen as a brain or biological dysfunction, but not as a necessarily lifelong condition like bipolar?” How exactly did they determine that this is a biological dysfunction? Is it just the assumption that if symptoms are severe and difficult to manage, it must be a brain malfunction?
The article ends with the following two paragraphs:
Of course there is no way to predict what practical effects creating the TDD category might have. For instance, Carlson points out that even if they are successful at changing the label that clinicians use, it could be that the kids all get the same medications as before. “They may get many of the same. Absolutely,” she says. “But the difference is going to be that you won’t have to take this for the rest of your life.”
Carlson doesn’t necessarily see this as a bad thing. She emphasizes that these children have very serious problems, and though there’s been trouble naming it, there’s clearly some sort of dysfunction in their brain. Shaffer agrees. “I don’t think anyone is arguing that these are perfectly normal children that get the label [bipolar] — far from it,” he says. “We’re saying these kids are very sick. But they probably don’t have bipolar disorder. And they probably do deserve a name that adequately describes what they’re doing.”
I’m not arguing that these kids are “perfectly normal,” but I do take issue with the idea that a team of psychiatrists can create a new category and say without any evidence that the problem they are attempting to describe has its root causes in biological dysfunction. Am I the only one who finds this approach both arbitrary and dogmatic? I believe these kids deserve more than a name that fits their symptoms. They deserve an approach directed at understanding the nature and cause of whatever it is they are suffering from.
We still have another 3 years to go before the DSM-V is published. It will be interesting to see if this the unofficial diagnosis comes into common use before then.