Auch dies hier kann ich leider erst frühestens Ende nächster Woche auf Deutsch zusammenfassen, falls nicht jemand anderes vorher die Zeit dafür findet.
Die Public Library of Science (PLoS, http://www.plos.org/), die schon letzten Herbst nachgewiesen hat, dass die Hypothese vom Serotonin-Mangel als Ursache von Depressionen durch nichts belegt ist (http://www.mut-zum-anderssein.de/PDF/Se ... othese.pdf), hat eine neue Studie zum Thema Antidepressiva veröffentlicht, unter der Fragestellung: "Heilen Antidepressiva oder erzeugen sie im Gehirn einen anormalen Zustand?" Ergebnis der Studie: Antidepressiva führen zu einer Besserung von Depressionen durch Manipulation der Hirnbotenstoffe hin zu einem anormalen Spiegel, wirken also wie Rauschdrogen, nicht wie Heilmittel. Sie bringen den Hirnstoffwechsel also nicht ins Gleichgewicht, wie den Patienten immer erzählt wird, sondern ins Ungleichgewicht. Der Begriff "Antidepressiva" solle darum ersetzt werden.
Die Studie findet sich hier:
http://dx.doi.org/10.1371/journal.pmed.0030240
bzw. hier:
http://medicine.plosjournals.org/perlse ... %2E0030240
Hier zwei englischsprachige Zusammenfassungen der Studie:
http://groups.yahoo.com/group/psychiatr ... e/7172?l=1
Do Antidepressants Cure or Create Abnormal Brain States?
Joanna Moncrieff, David Cohen
Joanna Moncrieff is a senior lecturer in Psychiatry, University College London, London, United Kingdom. David Cohen is a professor at the School of Social Work, College of Health and Urban Affairs, Florida International University, Miami, Florida, United States of America.
Funding: The authors received no funding to write this article.
Competing Interests: Joanna Moncrieff is Co-Chairperson of the Critical Psychiatry Network, a group of psychiatrists who dispute the predominance of biological models of mental disorder and campaign for a less coercive psychiatry.
Published: June 6, 2006
DOI: 10.1371/journal.pmed.0030240
Copyright: © 2006 Moncrieff and Cohen. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abbreviations: RCT, randomised controlled trial; SSRI, selective serotonin reuptake inhibitor; TCA, tricyclic antidepressant
Citation: Moncrieff J, Cohen D (2006) Do Antidepressants Cure or Create Abnormal Brain States? PLoS Med 3(7): e240
The term antidepressant refers to a drug that helps to rectify specific biological abnormalities that give rise to the symptoms of depression. This exemplifies what we have called the "disease-centred" model of psychotropic drug action. Modelled on paradigmatic situations in general medicine-such as the use of insulin in diabetes, antibiotics in infectious disease, chemotherapy in cancer-the disease-centred model suggests that antidepressants help restore normal functioning by acting on the neuropathology of depression or of depressive symptoms.
In contrast, we propose in this Essay that an alternative "drug-centred" model can better explain observed drug effects in psychiatric conditions. This drug-centred model suggests that instead of relieving a hypothetical biochemical abnormality, drugs themselves cause abnormal states, which may coincidentally relieve psychiatric symptoms (Table 1).
Alcohol's disinhibiting effects may relieve symptoms of social phobia, but that does not imply that alcohol corrects a chemical imbalance underlying social phobia. Sedation may lessen high arousal, present in many acute psychiatric situations. Drugs that induce indifference, such as neuroleptics or opiates, may help reduce the distress of acute psychotic symptoms. Low-dose stimulants may help improve attention and concentration in the short term.
The disease-centred model in psychiatry leads researchers to infer antidepressant effects from patients' scores on symptom rating scales presumed to assess the manifestations of the disease. The drug-centred model, on the other hand, suggests that physiological and subjective effects of drugs should be examined in their own right. These effects include various forms of sedation, stimulation, and a plethora of biopsychological states. Depending on individual inclination and context (including a person's emotional state upon drug ingestion), intoxication with some drugs produces euphoria or mood elevation. Because tolerance develops, however, euphoriant effects do not persist with long-term use.
If antidepressants or any other psychotropic drugs could be shown to have mood-elevating effects that were long-term and not diminished by being in a depressed emotional state, this would distinguish them from psychotropic drugs that cause euphoria and might prove uniquely useful in depressed patients.
Posted by
Robert Karl Stonjek
*******************
Alliance for Human Research Protection
http://www.ahrp.org/index.php
Contact: Vera Hassner Sharav, 212-595-8974, veracare@ahrp.org
In their provocative essay, Dr. Joanna Moncrieff of University College London and Professor David Cohen* of Florida International University in Miami, challenge the "disease-based" paradigm in psychiatry, arguing that the class of drugs known as antidepressants, and indeed all psychotropic drugs, produce their desired effects by creating abnormal brain states.
Psychotropic drugs induce sedation, or stimulation, or indifference, or a "plethora of psychobiological states," and may thus coincidentally relieve symptoms of psychiatric disorders. But Drs. Moncrieff and Cohen write that this in no way suggests that patients have "chemical imbalances" and they warn that these drug-induced states, though usually short-lived and may create more problems than they solve.
Drs. Moncrieff and Cohen argue that psychiatry's dominant "disease-centered model"-which holds that drugs correct "biochemical imbalances"-is far from established, and this for several reasons.
In the case of antidepressants, Moncrieff and Cohen show that all studies have failed to support the existence of pre-existing brain abnormalities among psychiatric patients. Animal models that try to mimic mental disorders fail to select drugs that are supposed to be effective for these disorders. In clinical trials testing antidepressants, rating scales include many items that would respond to any drug with sedative effects, thus outperforming placebos, but not because the drugs have specific "antidepressant" properties. Also, several other types of drugs, including benzodiazepines, antipsychotics, opiates, and others have been found to relieve depressive symptoms in controlled clinical trials.
Moncrieff and Cohen also show that so-called antidepressants affect healthy volunteers just like they do psychiatric patients-which weakens the idea that patients have abnormal brains. Finally, the authors remind us that the widespread use of so-called antidepressants, which are supposedly disorder-specific-"selective serotonin reuptake inhibitors"-have not led to demonstrable improvements in short or long-term outcomes of depression.
Drs. Moncrieff and Cohen propose instead that a "drug-centered model" best explains observed effects of antidepressants, in clinical trials and in ordinary patients' lives. They suggest that most tricyclic antidepressants are very sedating and produce EEG disturbances, causing cognitive dysfunctions. SSRIs appear to be mildly stimulating and sedative simultaneously, but can also have effects that progress to "frank agitation." In addition, these various drugs may share antipsychotics' and opiates' particularly blunting effects. Together, these sedative and stimulating effects explain antidepressants' popularity and perceived "effectiveness" among their users.
Moncrieff and Cohen warn that some drugs cause euphoria among some users, but this comes at a cost: "Drugs known to produce short-term euphoria require an increasing dose to maintain this effect (tolerance) and are associated with a compensatory dysphoria on discontinuation."
Tolerance requiring increased dose confirms the drugs pose a risk of drug-dependency (or addiction). "So far, however, there is no compelling evidence that there exists any drug induced effect consisting of a sustained elevation of mood."
Moncrieff and Cohen conclude as follows: "Many patients are led to believe by their physicians and by advertising that antidepressant drugs will act on the biological cause of their depressed state by rectifying a 'chemical imbalance'. On the contrary, our analysis indicates that there are no specific antidepressant drugs, that most short term effects of antidepressants are shared by numerous other drugs and that long term drug treatment with antidepressants or anything else has not been shown to lead to elevation of mood. We suggest the term "antidepressant" should be abandoned."
* Dr. David Cohen serves as Secretary on the board of directors of AHRP.