Re: "Medical model" in psychiatry/psychotherapy

[SMNagel29]

oops. . .should have read Allen's detailed contribution to this discussion before hitting the send button. . . Nonetheless, my interpretation of the data from a wide range of disciplines is supportive, I believe, of a monistic perspective in which the physiological cannot be disentangled from the behavioral/psychological when considering either etiology or treatment of even 'nebulous' conditions. (Although I believe that caution must be applied when using either treatment approach as both are fraught with uncertainties and potential for iatrogenic results.) I believe that we can migraine (and its associated psychological correlates) to the list of conditions in the recent abstract.   So. . . .  is this a medical model? . . .I best get back to work.   Sandra       Psychopharmacology (Berl). 2004 Aug;174(4):463-76. Epub 2004 Apr 16.     Human genetics of plasma dopamine beta-hydroxylase activity: applications to research in psychiatry and neurology. Cubells JF, Zabetian CP. Department of Psychiatry, Yale University School of Medicine and VA Connecticut Health Care System, 950 Campbell Avenue, West Haven, CT 06516, USA. [EMAIL PROTECTED] RATIONALE: Norepinephrine (NE) is a key neurotransmitter in the central and peripheral nervous systems. Dopamine beta-hydroxylase (DbetaH) catalyzes the synthesis of NE from dopamine (DA) and occurs in the plasma as a stable heritable trait. Studies of this trait have been useful in psychiatric and neurological research. OBJECTIVE: To selectively and critically review the literature on plasma DbetaH, and on recent progress understanding the molecular genetic basis for its inheritance. Based on this review, directions for future research in psychiatry and neurology will be suggested. METHODS: We selectively review the literature on the biochemical and molecular genetics of plasma DbetaH activity, as well as research on plasma and cerebrospinal fluid (CSF) DbetaH in psychiatric and neurological disorders. RESULTS: Strong evidence implicates DBH, the structural locus encoding DbetaH enzyme, as the major quantitative trait locus influencing plasma DbetaH activity, with one single nucleotide polymorphism (SNP) accounting for up to 50% of the variance. Mutations at DBH appear to be responsible for the rare syndrome of DbetaH deficiency. Some biochemical and genetic studies suggest associations between low plasma or CSF DbetaH and psychotic symptoms in several psychiatric disorders. Studies combining genotyping at DBH with biochemical measurement of plasma DbetaH have proven useful in studies of schizophrenia, cocaine-induced paranoia (CIP), depression, attention deficit hyperactivity disorder, and alcoholism. Such studies may also elucidate the contribution of noradrenergic dysfunction to a variety of symptoms in Parkinson's disease and other degenerative neurological disorders. CONCLUSIONS: A model is proposed, in which lower levels of DbetaH protein may lead to elevated ratios of DA to NE. This model may explain associations between lower plasma DbetaH activity and vulnerability to psychotic symptoms. Genotype-controlled analysis of plasma DbetaH holds promise for promoting further progress in research on psychiatric and neurological disorders. PMID: 15088079 [PubMed - in process]   In a message dated 12/4/2004 4:27:30 AM Eastern Standard Time, [EMAIL PROTECTED] writes: On 3 December Stephen Black wrote [snip]: >Perhaps doctors don't need to distinguish between them >because they only use one of these approaches (not really >true, as many dabble in psychodynamic explanation). But >in psychology some of us use one of these approaches and >others, the other. For example, a psychologist using the true > medical model might propose that schizophrenia is caused >by a gene on chromosome 7. Another psychologist using the >quasi-medical model might propose that schizophrenia is caused >by a defective personality resulting from maternal rejection. Surely the situation is not as straightforward as this passage of Stephen's seems to imply. But I suspect he was only putting it this way for didactic purposes. At any rate, I doubt Stephen will disagree, in general terms, with what I write in (a) below. At root I'm concerned about the idea that someone might contend that "schizophrenia is *caused* by a gene on chromosome x". (a) In a mental disorder such as schizophrenia there may be (almost certainly are) a number of factors, e.g., genetic propensity, occurrences in the womb before birth, adverse life experiences, regular ingesting of "recreational" drugs in susceptible individuals, and so on. (b) Most people who seek out psychotherapy do so to relieve symptoms that may be (relatively) less clear-cut than in the case of severe mental conditions like schizophrenia or bipolar disorder. These may range from severe depression, which may be closer to the kind of situation in the above cases, to more nebulous emotional/behavioural symptoms. In the latter cases there are no generally accepted views about the origins of the problems, nor, of course, of the means of relieving them. Explanations may come in various shapes and sizes, and it is surely one of the tasks of academic psychologists to critically examine such explanations for their plausibility, and, perhaps more important, the extent to which they are genuinely evidence-based. I'm not clear that mental/emotional disorders, at least of the more nebulous type, lend themselves to discussion in terms of "medical models". Better, to my mind, to critically examine each attempt at explanation, or more general explanatory system, on its merits. Allen Esterson Former lecturer, Science Department Southwark College, London [EMAIL PROTECTED] http://www.human-nature.com/esterson/index.html http://www.butterfliesandwheels.com/articleprint.php?num=10 http://www.butterfliesandwheels.com/articleprint.php?num=57 http://www.butterfliesandwheels.com/articleprint.php?num=58 http://www.psychiatrie-und-ethik.de/infc/1_gesamt_en.html   ******************************************************          Sandra M. Nagel, Ph.D.          Associate Professor, Psychology          Saginaw Valley State University          166 Brown Hall          7400 Bay Road          University Center, MI 48710 http://www.svsu.edu/~smnagel/research/          Office: (989) 964-4635          Fax: (989) 790-7656          E-Mail: [EMAIL PROTECTED] *************************************************** --- You are currently subscribed to tips as: archive@jab.org To unsubscribe send a blank email to [EMAIL PROTECTED]