Biopsychiatry controversy

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The biopsychiatry controversy is a dispute over which viewpoint should predominate and form the scientific basis of psychiatric theory and practice. The debate is a criticism of a claimed strict biological view of psychiatric thinking. Its critics include disparate groups such as the antipsychiatry movement and some academics.

Overview of opposition to biopsychiatry[edit]

Over centuries of progress medical science has developed a variety of therapeutic practices that have made many illnesses more treatable or even fully eradicable. Biological psychiatry or biopsychiatry aims to investigate determinants of mental disorders devising remedial measures of a primarily somatic nature.

This has been criticized by Alvin Pam for being a "stilted, unidimensional, and mechanistic world-view", so that subsequent "research in psychiatry has been geared toward discovering which aberrant genetic or neurophysiological factors underlie and cause social deviance".[1] According to Pam the "blame the body" approach, which typically offers medication for mental distress, shifts the focus from disturbed behavior in the family to putative biochemical imbalances.

Research issues[edit]

Current status in biopsychiatric research[edit]

Biopsychiatric research has produced reproducible abnormalities of brain structure and function, and a strong genetic component for a number of psychiatric disorders (although the latter has never been shown to be causative, merely correlative). It has also elucidated some of the mechanisms of action of medications that are effective in treating some of these disorders. Still, by their own admission, this research has not progressed to the stage that they can identify clear biomarkers of these disorders.

Research has shown that serious neurobiological disorders such as schizophrenia reveal reproducible abnormalities of brain structure (such as ventricular enlargement) and function. Compelling evidence exists that disorders including schizophrenia, bipolar disorder, and autism to name a few have a strong genetic component. Still, brain science has not advanced to the point where scientists or clinicians can point to readily discernible pathologic lesions or genetic abnormalities that in and of themselves serve as reliable or predictive biomarkers of a given mental disorder or mental disorders as a group. Ultimately, no gross anatomical lesion such as a tumor may ever be found; rather, mental disorders will likely be proven to represent disorders of intercellular communication; or of disrupted neural circuitry. Research already has elucidated some of the mechanisms of action of medications that are effective for depression, schizophrenia, anxiety, attention deficit, and cognitive disorders such as Alzheimer's disease. These medications clearly exert influence on specific neurotransmitters, naturally occurring brain chemicals that effect, or regulate, communication between neurons in regions of the brain that control mood, complex reasoning, anxiety, and cognition. In 1970, The Nobel Prize was awarded to Julius Axelrod, Ph.D., of the National Institute of Mental Health, for his discovery of how anti-depressant medications regulate the availability of neurotransmitters such as norepinephrine in the synapses, or gaps, between nerve cells.

American Psychiatric Association, Statement on Diagnosis and Treatment of Mental Disorders[2]

Focus on genetic factors[edit]

Researchers have proposed that most common psychiatric and drug abuse disorders can be traced to a small number of dimensions of genetic risk[3] and reports show significant associations between specific genomic regions and psychiatric disorders.[4][5] Though, to date only a few genetic lesions have been demonstrated to be mechanistically responsible for psychiatric conditions.[6][7] For example, one reported finding suggests that in persons diagnosed as schizophrenic as well as in their relatives with chronic psychiatric illnesses, the gene that encodes phosphodiesterase 4B (PDE4B) is disrupted by a balanced translocation.[8]

The reasons for the relative lack of genetic understanding is because the links between genes and mental states defined as abnormal appear highly complex, involve extensive environmental influences and can be mediated in numerous different ways, for example by personality, temperament or life events.[9] Therefore while twin studies and other research suggests that personality is heritable to some extent, finding the genetic basis for particular personality or temperament traits, and their links to mental health problems, is "at least as hard as the search for genes involved in other complex disorders."[10] Theodore Lidz[11] and The Gene Illusion.[12][13] argue that biopsychiatrists use genetic terminology in an unscientific way to reinforce their approach. Joseph maintains that biopsychiatrists disproportionately focus on understanding the genetics of those individuals with mental health problems at the expense of addressing the problems of the living in the environments of some extremely abusive families or societies.[14]

Focus on biochemical factors[edit]

The chemical imbalance hypothesis states that a chemical imbalance within the brain is the main cause of psychiatric conditions and that these conditions can be improved with medication which corrects this imbalance. In this hypothesis, emotions within a "normal" spectrum reflect a proper balance of neurochemicals, but abnormally extreme emotions, such as clinical depression, reflect an imbalance. This conceptual framework has been challenged within the scientific community, although no other demonstrably superior hypothesis has emerged. While the hypothesis has been shown to be simplistic and lacking (especially regarding psychotropic drugs with novel mechanisms such as tianeptine),[15] there is sufficient evidence to consider it as a useful heuristic in the aiding of our understanding of brain chemistry and explaining pharmacotherapy.[16][17] On the other hand, Elliot Valenstein, a psychologist, neuroscientist and prominent critic of biopsychiatry, states that the broad biochemical assertions and assumptions of mainstream psychiatry are not supported by evidence.[18]

Reductionism[edit]

Niall McLaren emphasizes in his books Humanizing Madness and Humanizing Psychiatry that the major problem with psychiatry is that it lacks a unified model of the mind and has become entrapped in a biological reductionist paradigm. The reasons for this biological shift are intuitive as reductionism has been very effective in other fields of science and medicine. However, despite reductionism's efficacy in explaining the smallest parts of the brain this does not explain the mind, which is where he contends the majority of psychopathology stems from. An example would be that every aspect of a computer can be understood scientifically down to the very last atom, however this does not reveal the program that drives this hardware. He also argues that the widespread acceptance of the reductionist paradigm leads to a lack of openness to self-criticism and therefore halts the very engine of scientific progress.[19] He has proposed his own natural dualist model of the mind, the biocognitive model, which is rooted in the theories of David Chalmers and Alan Turing and does not fall into the dualist's trap of spiritualism.[20]

Economic influences on psychiatric practice[edit]

American Psychiatric Association president Steven S. Sharfstein has stated that when the profit motive of pharmaceutical companies and human good are aligned, that the results are mutually beneficial and that "Pharmaceutical companies have developed and brought to market medications that have transformed the lives of millions of psychiatric patients. The proven effectiveness of antidepressant, mood-stabilizing, and antipsychotic medications has helped sensitize the public to the reality of mental illness and taught them that treatment works. In this way, Big Pharma has helped reduce stigma associated with psychiatric treatment and with psychiatrists." However, too often "[t]he practice of psychiatry and the pharmaceutical industry have different goals and abide by different ethics." He states a number of concerns exacerbating this situation which he suggests require remedying, including:[21]

  • that the psychiatric profession has allowed the biopsychosocial model to become entirely dominated by biological factors;
  • a "broken health care system" that allows "many patients [to be] prescribed the wrong drugs or drugs they don't need";
  • "medical education opportunities sponsored by pharmaceutical companies [that] are often biased toward one product or another";
  • "[d]irect marketing to consumers [that] also leads to increased demand for medications and inflates expectations about the benefits of medications";
  • drug company gifts to doctors, that have become sufficiently problematical as to warrant legislative constraints; and
  • "drug companies [paying] physicians to allow company reps to sit in on patient sessions allegedly to learn more about care for patients and then advise the doctor on appropriate prescribing."

Nevertheless, Sharfstein concluded that "[a]s psychiatrists, we should all be grateful for the modern pharmacopia and the promise of even more improvements in the future."[21]

Pharmaceutical industry influence on the psychiatric profession[edit]

Studies have shown that medical students and residents are susceptible to undue influence from pharmaceutical companies due to the companies involvement in medical school programs.[22]

Certain antidepressants have been shown to have only a minimal effect, over that of a placebo, on patients. In an analysis of the efficacy data submitted to the U.S. Food and Drug Administration for approval of the six most widely prescribed antidepressants approved between 1987 and 1999, it was found that

Approximately 80% of the response to medication was duplicated in placebo control groups, and the mean difference between drug and placebo was approximately 2 points on the 17-item (50-point) and 21-item (62-point) Hamilton Depression Scale. Improvement at the highest doses of medication was not different from improvement at the lowest doses. The proportion of the drug response duplicated by placebo was significantly greater with observed cases (OC) data than with last observation carried forward (LOCF) data. If drug and placebo effects are additive, the pharmacological effects of antidepressants are clinically negligible. If they are not additive, alternative experimental designs are needed for the evaluation of antidepressants.[23]

In an essay on advertisements for anti-depressants published in PLoS Medicine, social work academic Jeffrey Lacasse and neuroanatomist Jonathan Leo state that, despite this, the chemical imbalance theory is promoted by the medical industry as an explanation to depression and that their medicines correct the chemical imbalance. They also state that there is some evidence that both patients and professionals are influenced by the advertisements and patients may get prescribed medicines when other interventions are more suitable.[24]

In a further article they state that chemical imbalance has also been cited in media as an important cause of depression despite a lack of scientific literature that shows this causality.[25]

See also[edit]

General[edit]

Groups critical of the biomedical paradigm[edit]

  • Mindfreedom - A group which advocates for "choice" regarding psychopharmaceuticals.
  • ICSPP (International Center for the Study of Psychiatry and Psychology)
  • isps (International Society for the Psychological Treatment of the Schizophrenias and other Psychoses)

External links[edit]

Criticisms from psychologists & the medical profession[edit]

  1. APA Fights Attempt to Limit Access to Psychoactive Drugs, American Psychiatric Association president Michelle Riba, M.D., M.S.
  2. Against Biologic Psychiatry - an article by David Kaiser, M.D., in Psychiatric Times (1996, Vol. XIII, Issue 12).
  3. Challenging the Therapeutic State - special issue of The Journal of Mind and Behavior (1990, Vol.11:3).
  4. Letter of Resignation from the American Psychiatric Association - from Loren R. Mosher, M.D., former Chief of Schizophrenia Studies at the National Institute of Mental Health.
  5. Memorandum from the Critical Psychiatry Network to the United Kingdom Parliament - Written evidence to the House of Commons Select Committee on Health, April 2005.

Methodological issues[edit]

  1. On the Limits of Localization of Cognitive Processes in the Brain - an essay by William R. Uttal, Professor Emeritus of Psychology at the University of Michigan, based on his book The New Phrenology (MIT Press, 2001).

References[edit]

  1. ^ Pam, Alvin (1995). "Biological psychiatry: science or pseudoscience?". In Colin Ross and Alvin Pam. Pseudoscience in Biological Psychiatry: Blaming the Body. NY: Wiley & Sons. pp. 7–84. ISBN 0-471-00776-5. 
  2. ^ APA statement on Diagnosis and Treatment of Mental Disorders, American Psychiatric Association, September 26, 2003
  3. ^ Most psychiatric disorders share a small number of genetic risk factors, VCU study shows, Virginia Commonwealth University
  4. ^ Pickard BS, Malloy MP, Clark L et al. (March 2005). "Candidate psychiatric illness genes identified in patients with pericentric inversions of chromosome 18". Psychiatric Genetics 15 (1): 37–44. doi:10.1097/00041444-200503000-00007. PMID 15722956. 
  5. ^ Macgregor S, Visscher PM, Knott SA et al. (December 2004). "A genome scan and follow-up study identify a bipolar disorder susceptibility locus on chromosome 1q42". Molecular Psychiatry 9 (12): 1083–1090. doi:10.1038/sj.mp.4001544. PMID 15249933. 
  6. ^ van Belzen MJ, Heutink P (2006). "Genetic analysis of psychiatric disorders in humans". Genes, Brain and Behavior 5 (Suppl 2): 25–33. doi:10.1111/j.1601-183X.2006.00223.x. PMID 16681798. 
  7. ^ Meyer-Lindenberg A, Weinberger DR (October 2006). "Intermediate phenotypes and genetic mechanisms of psychiatric disorders". Nature Reviews Neuroscience 7 (10): 818–827. doi:10.1038/nrn1993. PMID 16988657. 
  8. ^ Millar JK, Pickard BS, Mackie S et al. (November 2005). "DISC1 and PDE4B are interacting genetic factors in schizophrenia that regulate cAMP signaling". Science 310 (5751): 1187–1191. doi:10.1126/science.1112915. PMID 16293762. 
  9. ^ Kates WR (April 2007). "Inroads to mechanisms of disease in child psychiatric disorders". The American Journal of Psychiatry 164 (4): 547–551. doi:10.1176/appi.ajp.164.4.547. PMID 17403964. 
  10. ^ Van Gestel S, Van Broeckhoven C (October 2003). "Genetics of personality: are we making progress?". Molecular Psychiatry 8 (10): 840–852. doi:10.1038/sj.mp.4001367. PMID 14515135. 
  11. ^ Lidz T, Blatt S (April 1983). "Critique of the Danish-American studies of the biological and adoptive relatives of adoptees who became schizophrenic". The American Journal of Psychiatry 140 (4): 426–34. PMID 6837778. 
  12. ^ Joseph, Jay (2003). The Gene Illusion: Genetic Research in Psychiatry and Psychology Under the Microscope. New York, NY: Algora. ISBN 0-87586-344-2. [page needed]
  13. ^ Joseph, Jay (2006). The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes. NY: Algora Publishing. ISBN 0-87586-410-4. [page needed]
  14. ^ Jay Joseph The Missing Gene
  15. ^ McEwen BS, Chattarji S, Diamond DM et al. (August 2009). "The neurobiological properties of tianeptine (Stablon): from monoamine hypothesis to glutamatergic modulation". Molecular Psychiatry 15 (3): 237–249. doi:10.1038/mp.2009.80. PMC 2902200. PMID 19704408. 
  16. ^ Schildkraut JJ (November 1965). "The catecholamine hypothesis of affective disorders: a review of supporting evidence". The American Journal of Psychiatry 122 (5): 509–22. doi:10.1176/appi.ajp.122.5.509 (inactive 2010-01-05). PMID 5319766. 
  17. ^ Looking Beyond the Monoamine Hypothesis
  18. ^ Valenstein, Elliot (1998). Blaming the Brain: The Truth about Drugs and Mental Health. The Free Press. ISBN 0-684-84964-X. [page needed]
  19. ^ McLaren, Niall (2007). Humanizing Madness. Ann Arbor, MI: Loving Healing Press. pp. 3–21. ISBN 1-932690-39-5. 
  20. ^ McLaren, Niall (2009). Humanizing Psychiatry. Ann Arbor, MI: Loving Healing Press. pp. 17–18. ISBN 1-61599-011-9. 
  21. ^ a b Sharfstein, Steven S. (August 19, 2005). "Big Pharma and American Psychiatry: The Good, the Bad, and the Ugly". Psychiatric News (American Psychiatric Association) 40 (16): 3. Retrieved January 2008. 
  22. ^ Zipkin DA, Steinman MA (August 2005). "Interactions between pharmaceutical representatives and doctors in training. A thematic review". Journal of General Internal Medicine 20 (8): 777–786. doi:10.1111/j.1525-1497.2005.0134.x. PMC 1490177. PMID 16050893. 
  23. ^ Waring DR (December 2008). "The antidepressant debate and the balanced placebo trial design: an ethical analysis". International Journal of Law and Psychiatry 31 (6): 453–462. doi:10.1016/j.ijlp.2008.09.001. PMID 18954907. 
  24. ^ Lacasse JR, Leo J (December 2005). "Serotonin and depression: a disconnect between the advertisements and the scientific literature". PLoS Medicine 2 (12): e392. doi:10.1371/journal.pmed.0020392. PMC 1277931. PMID 16268734. 
  25. ^ Leo, Jonathan; Lacasse, Jeffrey R. (2007). "The Media and the Chemical Imbalance Theory of Depression". Society 45: 35–45. doi:10.1007/s12115-007-9047-3.