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What about alternative hypotheses?

Posted by framus on 28 Feb 2011 at 14:42 GMT

Although I share the authors' concerns about data misrepresentation, I think that their analysis does not fully support their conclusion that representations are biased in favour of biological explanations of ADHD. This is because the authors only looked for data that could confirm their viewpoint. What would be needed is to carry out a similar analysis for representations of non-biological explanations. If they are equally misrepresented, then misrepresentation problems remain but the ground is even, not biased.

No competing interests declared.

RE: What about alternative hypotheses?

Gonon replied to framus on 07 Mar 2011 at 15:12 GMT

Three types of discourses attempt to describe mental diseases and their etiology: i) biological psychiatry describes them in terms of brain disease, ii) psychopathology describes them in terms of defective psychological development, and iii) mental health sociology describes them in terms of social inequity. These discourses are not mutually exclusive. For example severe maltreatment during childhood, which is more frequent in family with low socioeconomic status, might cause during adulthood depression, anxiety and dysfunction of the corticotropic axis (see Hackman et al, (2010) Nat Rev Neurosci, 11: 651-659). In our article we show that the neuroscience discourse is distorted by data misrepresentation and publication biases. As you suggest, it is likely that the discourses of psychopathology and of mental health sociology also suffer from some forms of data misrepresentation. However, my colleagues and myself we are neuroscientists. Our field of expertise makes us capable to analyze the neuroscience discourse but not the two others.
Our article expresses no opinion about the relevance of these 3 discourses regarding ADHD. We are neuroscientists and we have written to neuroscientists to draw the attention of our colleagues on data misrepresentation and on its consequences regarding the understanding of mental diseases in the lay public. A recent study shows that "in 2006, 67 % of the public attributed major depression to neurobiological causes, compared with 54 % in 1996" (Pescosolido et al. 2010, Am J Psychiatry 167: 1321-1330). However, as Steven Hyman said in 2008 about psychiatry: "no new drug targets or therapeutic mechanisms of real significance have been identified for more than four decades" (Nature, 2009, 455: 890-893). Therefore, although decades of intense research did not significantly improve clinical psychiatry (see also Luciano, 2004, Molecular Psychiatry 9: 1), the neuroscience discourse affects the lay public. Unfortunately, holding a neurobiological conception of mental disease does not decrease stigma and increases community rejection in the lay public (Pescosolido et al, 2010). Therefore, our article is an attempt to draw the attention of the neuroscientist community about the ethics of neuroscience communication.
Francois Gonon

No competing interests declared.