John Read, Placebo


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John Read, Placebo

  1. 1. NZPsS Conference 2011 <ul><li>DOES IT MATTER IF ITS </li></ul><ul><li>MOSTLY A PLACEBO </li></ul><ul><li>EFFECT? </li></ul><ul><li>THE EFFICACY OF </li></ul><ul><li>ANTI-DEPRESSANTS </li></ul><ul><li>ANTI-PSYCHOTICS </li></ul><ul><li>AND ELECTROSHOCK THERAPY </li></ul><ul><li>Professor John Read </li></ul><ul><li>University of Auckland </li></ul><ul><li>[email_address] </li></ul>
  2. 2. PLACEBO EFFECTS <ul><li>Placebo = Latin for ‘I please’ </li></ul><ul><li>Instillation of hope </li></ul><ul><li>Expectancy of recovery </li></ul><ul><li>Operate on clients AND clinicians </li></ul>
  3. 3. Much Touted “Depression Risk Gene” May Not Add to Risk After All. New Look at Data Confirms Strong Association between Depression and Stressful Life Events <ul><li>Merikangas, K. Journal of the American Medical Association June 17, 2009, </li></ul><ul><li>Re-analyzing data on 14,250 participants in 14 studies . .. </li></ul><ul><li>… . found a strong association between the number of stressful life events and risk of depression across the studies. </li></ul><ul><li>However, the presumed high-risk version of the serotonin transporter gene did not show a relationship to increased risk for major depression, alone or in interaction with stressful life events. </li></ul>
  4. 5. ‘ Initial Severity and Antidepressant Benefits’ Kirsch et al. (2008) <ul><li>Meta-analysis of all available studies, including those previously kept secret by the drug companies: </li></ul><ul><li>Drug–placebo differences: </li></ul><ul><li>Virtually no difference at moderate levels of initial depression </li></ul><ul><li>Small difference for patients with very severe initial depression . . . </li></ul><ul><li>. . . reaching ‘clinical significance’ only for patients at the upper end of the very severely depressed category. </li></ul>
  5. 6. Most Common Adverse effects of anti-depressants <ul><li>Nausea 22% </li></ul><ul><li>Headache 21%   </li></ul><ul><li>Insomnia 19% </li></ul><ul><li>Nervousness 13% </li></ul><ul><li>Anxiety 12%   </li></ul><ul><li>Somnolence 12%   </li></ul><ul><li>Asthenia 11%  </li></ul><ul><li>Diarrhea 11%   </li></ul><ul><li>Anorexia 10% </li></ul>
  6. 7. No evidence of genetic predisposition to schizophrenia (Hamilton, 2008, American Journal of Psychiatry) <ul><li>‘ The most comprehensive genetic association study of genes previously reported to contribute to the susceptibility to schizophrenia’ found that ‘none of the polymorphisms were associated with the schizophrenia phenotype at a reasonable threshold for statistical significance’ </li></ul><ul><li>‘ The distribution of test statistics suggests nothing outside of what would be expected by chance’ </li></ul>
  7. 8. Cochrane review of Risperidone (Rattehalli, Jayaram, & Smith, 2010). <ul><li>“ Risperidone appears to have a marginal benefit in terms of clinical improvement compared with placebo in the first few weeks of treatment but the margin of improvement may not be clinically meaningful. </li></ul><ul><li>Global effects suggests that there is no clear difference between risperidone and placebo </li></ul><ul><li>Risperidone causes many adverse effects and, these effects are important and common. </li></ul><ul><li>People with schizophrenia or their advocates may want to lobby regulatory authorities to insist on better studies being available before wide release of a compound with the subsequent beguiling advertising.” </li></ul>
  8. 10. Antipsychotic Drugs <ul><li>Adverse Effects </li></ul><ul><li>Traditional antipsychiotics: </li></ul><ul><li>Tardive Dyskinesia (20-50%) </li></ul><ul><li>irreversible in two-thirds </li></ul><ul><li>Neuroleptic Malignant Syndrome (often fatal) (1-2%) </li></ul><ul><li>New ‘atypical’ antipsychotics: </li></ul><ul><li>F.D.A. ‘no safer or more effective’ </li></ul><ul><li>Agranulocytosis </li></ul><ul><li>Weight gain </li></ul><ul><li>Diabetes </li></ul><ul><li>Sexual dysfunction </li></ul><ul><li>Neurodegeneration </li></ul><ul><li>Mortality ? </li></ul>
  9. 11. Influence of antipsychotics on mortality in schizophrenia: Systematic review Weinmann, S., Aderhold, V., Read, J. Schizophrenia Research (2009) <ul><li>Only 12 studies met the inclusion criteria. </li></ul><ul><li>Three out of five studies examining antipsychotic dosage and higher mortality showed a significant association for one or more antipsychotics. </li></ul><ul><li>Two out of four found negative effects of antipsychotic polypharmacy on life-expectancy </li></ul><ul><li>A major confounding factor may be a higher risk factor load for somatic disorders in the most severely mentally ill. </li></ul><ul><li>Conclusion: There is some evidence that long-term exposure to antipsychotics increases mortality in schizophrenia. </li></ul><ul><li>More rigorously designed, prospective studies are urgently needed. </li></ul>
  10. 12. Long-term Antipsychotic Treatment and Brain Volumes A Longitudinal Study of First-Episode Schizophrenia Ho,B et al. ARCH GEN PSYCHIATRY/VOL 68 (NO. 2), FEB 2011 <ul><li>Greater intensity of antipsychotic treatment was associated with indicators of generalized and specific brain tissue reduction after controlling for effects of 3 predictors. </li></ul><ul><li>More antipsychotic treatment was associated with smaller gray matter volumes. </li></ul><ul><li>Progressive decrement in white matter volume was most evident among patients who received more antipsychotic treatment. </li></ul>
  11. 13. The public prefer psychotherapy to anti-psychotic drugs in: <ul><li>Australia </li></ul><ul><li>Austria </li></ul><ul><li>Canada </li></ul><ul><li>China </li></ul><ul><li>England </li></ul><ul><li>Germany </li></ul><ul><li>Hong Kong </li></ul><ul><li>India </li></ul><ul><li>Italy </li></ul><ul><li>Japan </li></ul><ul><li>Russia </li></ul><ul><li>South Africa </li></ul><ul><li>Slovakia </li></ul><ul><li>Switzerland </li></ul><ul><li>Turkey </li></ul><ul><li>Read J (2007) Australian Psychologist </li></ul>
  12. 14. Why the public rejects anti-psychotic medication <ul><li>Australia (Jorm et al., 2000) </li></ul><ul><li>‘ have more risks than benefits’ </li></ul><ul><li>‘ lack efficacy because they do not deal with the roots of the problem’ </li></ul><ul><li>‘ are prescribed for the wrong reasons (e.g., to avoid talking about problems, as a straight jacket)’ </li></ul>
  13. 16. The effectiveness of electroconvulsive therapy: A literature review JOHN READ and RICHARD BENTALL Epidemiologia e Psichiatria Sociale, 19, 4, 2010 <ul><li>Placebo controlled studies show minimal support for </li></ul><ul><li>effectiveness with either depression or </li></ul><ul><li>schizophrenia’ during the course of treatment (i.e. </li></ul><ul><li>only for some patients, on some measures, </li></ul><ul><li>sometimes perceived only by psychiatrists but not by </li></ul><ul><li>other raters), and no evidence , for either diagnostic </li></ul><ul><li>group, of any benefits beyond the treatment </li></ul><ul><li>period . </li></ul><ul><li>There are no placebo-controlled studies evaluating </li></ul><ul><li>the hypothesis that ECT prevents suicide , and no </li></ul><ul><li>robust evidence from other kinds of studies to </li></ul><ul><li>support the hypothesis. </li></ul><ul><li>Given the strong evidence of persistent and, for </li></ul><ul><li>some, permanent brain dysfunction , primarily </li></ul><ul><li>evidenced in the form of retrograde and </li></ul><ul><li>anterograde amnesia, and the evidence of a slight </li></ul><ul><li>but significant increased risk of death , the cost- </li></ul><ul><li>benefit analysis for ECT is so poor that its use </li></ul><ul><li>cannot be scientifically justified. </li></ul>
  14. 17. <ul><li>The role of psychologists? </li></ul><ul><li>Ethical principle of INFORMED CONSENT </li></ul>