What should be said to the lay public regarding ADHD etiology based on unbiased systematic quantitative empirical evidence


  • How to Cite this Article: Cortese S, Faraone SV, Sergeant J. 2011. What Should Be Said to the Lay Public Regarding ADHD Etiology Based on Unbiased Systematic Quantitative Empirical Evidence. Am J Med Genet Part B 156:987–988.

Reply to Gonon et al.:

We welcome the clarifications that Gonon and coworkers have made in their letter to the editor and support their main conclusion that ADHD is caused by “a combination of biological and social factors,” a view which is well consolidated in the ADHD scientific community [Biederman and Faraone, 2005; Sergeant, 2005; Nigg et al., 2010]. We also share with Gonon and colleagues the concern that the media may misreport articles in scientific journals, and that unbalanced statements in the scientific literature concerning genetic or environmental factors could also lead to incorrect and misleading reports by media.

We continue to disagree with the statement in the PLoS ONE paper [Gonon et al., 2011] that “Data misrepresentations are frequent (italics by the authors) in the scientific literature dealing with ADHD.” Gonon and coworkers believe we have focused, in an “unfair way,” only on one misrepresentation, overlooking the other two types of misrepresentation that, according to them, are more frequent and would, therefore, strongly support their claims. We have two concerns about these two types of misrepresentation: (1) how they are defined and (2) the nature of how they were reviewed by Gonon et al. [2011].

Gonon et al. [2011] defined “fact omission” as follows: “This misrepresentation consists of putting in the summary a fixed conclusion while raw data, which strongly limit the relevance of this conclusion are only given in the results section.” We agree that conclusions should be tempered by the level of uncertainty in the data, but it seems unfair to accuse a colleague of misrepresentation if all the data have been accurately presented in the manuscript. The other type of misrepresentation was “extrapolating basic and pre-clinical findings to new therapeutic prospects.” This is based on the premise that “investigations based on mouse behavior cannot capture the ADHD complexity” and thus cannot be used to draw conclusions about therapeutic prospects. Although it is reasonable for Gonon et al. [2011] to question the validity of animal models of ADHD, there are different views about the validity of these methods, which should be viewed as honest differences of opinion rather than misrepresentation.

Our second concern about these two types of alleged misrepresentation is that a small amount of data has been used to assert a strong conclusion. Their data about “fact omission” concerns only one of the many genes studied in ADHD (DRD4). Their discussion of “inappropriate extrapolation to therapeutic prospects” concerns 23% of papers in a small area of ADHD research, namely, animal models. These fragmentary and, as recognized by Gonon et al. [2011], “qualitative” examples do not support the statement that data are frequently misrepresented in ADHD scientific literature, even if one accepts their definition of misrepresentation. It is premature to accuse colleagues of misrepresentation, based on a small qualitative review. A systematic, comparative, and quantitative review of all the relevant literature would be necessary to support such statements. A review of papers on one gene and 23% of studies in a particular field of research is insufficient to conclude that “Data misrepresentations are frequent in the scientific literature dealing with ADHD.”

We thank and support Dr. Gonon and colleagues for reminding the scientific community that an important duty of the researchers is to consider the implications their work might have when disseminated to the lay public or to clinical colleagues who do not fully understand the intricacies of research methodology. We hope that future studies of this issue use a systematic, quantitative, and unbiased analysis of the empirical evidence, much of which is existent in published meta-analyses of the neurobiology of ADHD [Cortese et al., 2011].