It goes without saying that we
cannot have a successful treatment regime without first establishing in concrete
specific form the nature, mode and aetiology of the particular ailment. With
regard to bipolar disorder, it may be noted that some 40 yrs ago a series of
experimental approaches known as discriminant function analysis were
carried out to determine in more precise fashion the differences between the
major psychiatric disorders - bipolar and schizophrenia. One such study, by
Kendall and Gourlay in 1970, compiled the symptoms of 300 patients who had been
previously diagnosed with both schizophrenia and bipolar disorder. Assigning
negative scores to 'schizophrenic' symptoms and positive scores to those given
an affective (ie bipolar) diagnosis it was found that most patients fell in the
middle range, close to zero, indicating the existence of a continuum rather than
the presence of two discrete illnesses. More comprehensive analyses where then
carried out and in like fashion unearthed similar findings.
This embarrassing overlap, from the point of view of diagnostic clarity, saw its attempted resolution through the creation of a new medical entity; schizoaffective disorder but this itself found difficulty in being accepted because of the power and influence of the original Kraepelinian dichotomy of the old paranoias into the affective (manic-depression/bipolar) and cognitive (schizophrenia) disorders.
In fact, much can gleaned from the response of the compilers of the American Psychiatric Association's Diagnostic and Statistical Manual; instead of proposing a fundamental re-evaluation of their theoretical suppositions they have instead responded with a further proliferation of diagnostic categories.
Perhaps the most crucial upshot of this diagnostic uncertainty is the implications it has for guiding treatment and research; a difficulty already foreseen by Alfred Meyer who once said; 'we should give up the idea of classifying people as we do plants'. He objected to the notion that a diagnosis was believed to lead automatically to a choice of treatment. For which 'schizophrenic', or 'bipolar' after all, is receiving the MRI scan that will indicate 'structural' or 'functional abnormalities'? Is it the senile, almost autistic version espoused by Emil Kraepelin or the linguistically-challenged, emotionally discordant subject of Eugen Bleuler? Or is it in fact a hazy conflation of both these signifieds?
It's clear that what we are presented with as a 'disease', that is to say what is commonly understood by the term is that of a physical defect that impairs the normal functioning of the organism. Viewed from the vantage point of someone who hasn't been afflicted with the designation 'bipolar' or 'schizophrenic' the constructed symptomatology, to the casual observer at least, does indeed appear sufficiently unattractive as to warrant the description of an 'illness'; on the one hand we are told of 'social withdrawal', lack of motivation' and 'low energy levels' and on the other we have the equally subjectively determined appellations of 'manic exuberance', 'ideas of reference', 'delusional ideation' and so on. In schizophrenia, the first set of descriptive categories are referred to as the negative symptoms and the latter regarded as the so-called positive symptoms. Likewise, almost the same sets of descriptions are respectively associated in the case of bipolar disorder with the so-called 'low' and 'high' phases.
There is a much easier explanation of course for all this confusion and that is that people called bipolar or schizophrenic haven't got any discernible abnormalities, disease or defects in the first place and this is evidenced by the simple fact that there are no tests available which indicate a structural or functional difference between their brains and that of the normal populace. However, this is not to say these people haven't got problems in living, problems which cannot conceivably improve if arguments such as the following are allowed to gain currency;
Should people (and foetuses) have their mood genes examined to assess their predisposition to mood disorders? Will new treatments of mood disorders adversely affect positive character traits such as creativity? - Samuel Barondes, Mood Genes
The first and most obvious assumption being made here is that extreme fluctuations in mood, in and of themselves, constitute not merely a 'disorder' but an 'illness' and 'disease'. From these assumptions that of course fly in the face of the avowed scientific methodology of deducting from solidly established first principles a prescriptive thematic is adopted throughout and the grand narrative of heroic scientific endeavour quickly supplants any lingering doubt of a connectivity between ideation, behaviour and any specific environmental triggers that may be present. These are terms that are used continuously throughout the work and the 'illness' or 'disease' rapidly become shorthand descriptions for the constructed set of symptoms that have become known as 'manic-depression' or, more lately, 'bipolar disorder'.
Now, in Mood Genes, Barondes makes an early declaration of interest;
'in the case of manic-depression for which there are some effective medications, such as lithium and Prozac, these drugs have many drawbacks. Treating a mood disorder with them is like treating an infection with aspirin: symptoms may be relieved but the fundamental problem remains unaddressed. Finding mood genes will change all this.'
Needless to say there are many social accolades and financial rewards awaiting for those who can demonstrate the efficacy of their work in conquering an outstanding social problem. And, of course, the greater the problem is perceived to be the greater will be the reward. In this case we see highlighted the competing claims of the pharmaceutical industry and a commercialized science of genetics. Some opponents of the medical model may regard the difference as only superficial given that both start off on the basis that the basic problem resides in an abnormal body chemistry.
Well, if geneticists discover, for instance, a region on a particular chromosome responsible for encoding the production of an amino acid that is involved in the metabolic pathway of a neurotransmitter that is found to be overabundant in a region of the brain of a patient who is in say, a 'manic state', and then after a course of gene therapy alter that chromosome to ensure that it no longer produces said acid, the change initiated becomes long-term and obviously renders superfluous the further intake of medication. For Barondes particular struggle here is to try and highlight the primary causative role of our genes and the relative efficacy of gene therapy over drug therapy.
So, if you were to regard the 'manic' symptoms as the manifestation of a 'disease' then the geneticists approach is entirely logical and would presumably mean in most cases the end of the drug-taking regimen. Simply isolate the 'pathogenic' substance, in this case, the area of the chromosome concerned with the production of our hypothetical amino acid, neutralize its capacity to produce, and then wait for the expected behavioural changes to occur. However, both geneticists and the advocates of pharmaceutical interventions are obviously protecting a vested interest in their declarations that the cause, the primum mobile of the observed behavioural differences lies in an altered biochemistry rather than residing in the person's subjective interaction with their environment.
The message as I'm receiving it is quite clear; there are those among us who feel so strongly and so deeply, who carry so hard the cross of an overly-inscribable body, that their capacity to engage in normal day to day activities has somehow become compromised. Can this though be said to be constitutive of a disease with an attendant battery of symptoms and treatment regimes or is it not rather a sentiment of being?
How, in fact, have we come to be so blinded that what we are confronted with are extremes of emotional states; love, joy, sadness, anger, frustration. It should be the task of any humanist intervention worthy of the name to register first the primacy of feelings over thinking and behaviour for it is the one that causes the other and the fact that we are on the verge of dabbling with gene therapy in a futile attempt to erase what are our most distinctively human traits is surely the apogee of a Promethean hubris.
This embarrassing overlap, from the point of view of diagnostic clarity, saw its attempted resolution through the creation of a new medical entity; schizoaffective disorder but this itself found difficulty in being accepted because of the power and influence of the original Kraepelinian dichotomy of the old paranoias into the affective (manic-depression/bipolar) and cognitive (schizophrenia) disorders.
In fact, much can gleaned from the response of the compilers of the American Psychiatric Association's Diagnostic and Statistical Manual; instead of proposing a fundamental re-evaluation of their theoretical suppositions they have instead responded with a further proliferation of diagnostic categories.
Perhaps the most crucial upshot of this diagnostic uncertainty is the implications it has for guiding treatment and research; a difficulty already foreseen by Alfred Meyer who once said; 'we should give up the idea of classifying people as we do plants'. He objected to the notion that a diagnosis was believed to lead automatically to a choice of treatment. For which 'schizophrenic', or 'bipolar' after all, is receiving the MRI scan that will indicate 'structural' or 'functional abnormalities'? Is it the senile, almost autistic version espoused by Emil Kraepelin or the linguistically-challenged, emotionally discordant subject of Eugen Bleuler? Or is it in fact a hazy conflation of both these signifieds?
It's clear that what we are presented with as a 'disease', that is to say what is commonly understood by the term is that of a physical defect that impairs the normal functioning of the organism. Viewed from the vantage point of someone who hasn't been afflicted with the designation 'bipolar' or 'schizophrenic' the constructed symptomatology, to the casual observer at least, does indeed appear sufficiently unattractive as to warrant the description of an 'illness'; on the one hand we are told of 'social withdrawal', lack of motivation' and 'low energy levels' and on the other we have the equally subjectively determined appellations of 'manic exuberance', 'ideas of reference', 'delusional ideation' and so on. In schizophrenia, the first set of descriptive categories are referred to as the negative symptoms and the latter regarded as the so-called positive symptoms. Likewise, almost the same sets of descriptions are respectively associated in the case of bipolar disorder with the so-called 'low' and 'high' phases.
There is a much easier explanation of course for all this confusion and that is that people called bipolar or schizophrenic haven't got any discernible abnormalities, disease or defects in the first place and this is evidenced by the simple fact that there are no tests available which indicate a structural or functional difference between their brains and that of the normal populace. However, this is not to say these people haven't got problems in living, problems which cannot conceivably improve if arguments such as the following are allowed to gain currency;
Should people (and foetuses) have their mood genes examined to assess their predisposition to mood disorders? Will new treatments of mood disorders adversely affect positive character traits such as creativity? - Samuel Barondes, Mood Genes
The first and most obvious assumption being made here is that extreme fluctuations in mood, in and of themselves, constitute not merely a 'disorder' but an 'illness' and 'disease'. From these assumptions that of course fly in the face of the avowed scientific methodology of deducting from solidly established first principles a prescriptive thematic is adopted throughout and the grand narrative of heroic scientific endeavour quickly supplants any lingering doubt of a connectivity between ideation, behaviour and any specific environmental triggers that may be present. These are terms that are used continuously throughout the work and the 'illness' or 'disease' rapidly become shorthand descriptions for the constructed set of symptoms that have become known as 'manic-depression' or, more lately, 'bipolar disorder'.
Now, in Mood Genes, Barondes makes an early declaration of interest;
'in the case of manic-depression for which there are some effective medications, such as lithium and Prozac, these drugs have many drawbacks. Treating a mood disorder with them is like treating an infection with aspirin: symptoms may be relieved but the fundamental problem remains unaddressed. Finding mood genes will change all this.'
Needless to say there are many social accolades and financial rewards awaiting for those who can demonstrate the efficacy of their work in conquering an outstanding social problem. And, of course, the greater the problem is perceived to be the greater will be the reward. In this case we see highlighted the competing claims of the pharmaceutical industry and a commercialized science of genetics. Some opponents of the medical model may regard the difference as only superficial given that both start off on the basis that the basic problem resides in an abnormal body chemistry.
Well, if geneticists discover, for instance, a region on a particular chromosome responsible for encoding the production of an amino acid that is involved in the metabolic pathway of a neurotransmitter that is found to be overabundant in a region of the brain of a patient who is in say, a 'manic state', and then after a course of gene therapy alter that chromosome to ensure that it no longer produces said acid, the change initiated becomes long-term and obviously renders superfluous the further intake of medication. For Barondes particular struggle here is to try and highlight the primary causative role of our genes and the relative efficacy of gene therapy over drug therapy.
So, if you were to regard the 'manic' symptoms as the manifestation of a 'disease' then the geneticists approach is entirely logical and would presumably mean in most cases the end of the drug-taking regimen. Simply isolate the 'pathogenic' substance, in this case, the area of the chromosome concerned with the production of our hypothetical amino acid, neutralize its capacity to produce, and then wait for the expected behavioural changes to occur. However, both geneticists and the advocates of pharmaceutical interventions are obviously protecting a vested interest in their declarations that the cause, the primum mobile of the observed behavioural differences lies in an altered biochemistry rather than residing in the person's subjective interaction with their environment.
The message as I'm receiving it is quite clear; there are those among us who feel so strongly and so deeply, who carry so hard the cross of an overly-inscribable body, that their capacity to engage in normal day to day activities has somehow become compromised. Can this though be said to be constitutive of a disease with an attendant battery of symptoms and treatment regimes or is it not rather a sentiment of being?
How, in fact, have we come to be so blinded that what we are confronted with are extremes of emotional states; love, joy, sadness, anger, frustration. It should be the task of any humanist intervention worthy of the name to register first the primacy of feelings over thinking and behaviour for it is the one that causes the other and the fact that we are on the verge of dabbling with gene therapy in a futile attempt to erase what are our most distinctively human traits is surely the apogee of a Promethean hubris.
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