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Dear Editor,

  1. Top of page
  2. Dear Editor,
  3. Acknowledgements
  4. REFERENCES

With Dr. Cortese and Dr. Sergeant you have published an editorial article [Cortese et al., 2011], which questions our recent study [Gonon et al., 2011]. We believe that your criticism is mainly based on an inaccurate account of our study. Indeed, we have clearly stated our aim in the introduction: “We do not question the data regarding ADHD and the validity of their interpretation. We examine how data are presented in scientific and media articles” [Gonon et al., 2011]. In other words our concern is not about the scientific knowledge per se, but about what it is said to the lay public regarding ADHD.

The first part of your article is aimed at rejecting “the anachronistic dichotomy between genetic and environmental factors” regarding ADHD etiology. To support your view, you have nicely summarized the available data about the genetics of ADHD. However, using wrong and incomplete citations of our article you state that we have defended this dichotomy. Actually, we agree with you and, in our article we have explicitly defended the view “that ADHD is caused by a combination of biological and social factors.” Dr. Sonuga-Barke has expressed our point of view even more accurately than we did: “Now, all but the most dogged of genetic determinists have revised their view of the primacy of genetic factors so as to encompass a central role for the environment in the development of mental disorder. This is the case even for the most heritable conditions. For instance, in my field, ADHD, despite the remarkable early advances using candidate gene approaches, subsequent progress has been slow: we are now using larger and larger samples of patients to demonstrate smaller and smaller molecular genetic main effects” [Sonuga-Barke, 2010].

In the second part of your article you question our opinion about the impact of the neurobiological discourse on ADHD treatment. You say: “We do not think that research in the neurobiology of ADHD favors the use of pharmacological treatments and we are not aware of any empirical study, systematic quantitative reviews or meta-analysis supporting this statement.” Again we agree with you that, in theory, the neurobiology of ADHD per se does not favor any treatment. However, although systematic studies are still lacking, we have already collected numerous examples in newspapers, textbooks, TV programs, web sites, and conferences presented to the lay public, in which the neurobiological observations were misrepresented to give an unbalanced support to psychostimulant treatment. For instance, the British newspaper “The Independent” published on February 1st, 2011 an article about ADHD with the following sentence: “Scientists believe it [ADHD] is caused by a lack of dopamine, the mood-regulating brain chemical, so clinicians prescribe drugs such as Ritalin to stimulate dopamine release.”

However, our main concern is related to your account of our observations in the two last paragraphs of your article. You extract a few sentences from our article in an unfair way to state that data misrepresentation is very infrequent and that our opposite point of view is not supported by sound empirical observations. Based on your unfair account, your conclusion brings discredit to our study: “Ironically, their article is an example of misrepresentation of scientific data” [Cortese et al., 2011].

Actually, we have described three types of misrepresentations: (i) internal inconsistencies between results and conclusions, (ii) omission of relevant facts, and (iii) inappropriate extrapolation to therapeutic prospects [Gonon et al., 2011]. We have reported that the first is hopefully infrequent: among 360 articles it affected only 2 studies, but the claimed conclusions of those 2 studies have been widely echoed in the media. However, the two other types of data misrepresentation were found to be much more frequent. The omission of relevant facts was observed in about 80% of the summaries in a systematic search of all 219 articles reporting on the association of ADHD with polymorphisms of the gene coding for the D4 dopamine receptor. Indeed, 80% of the summaries that put forward a significant association between this gene and ADHD, omitted to mention either the raw data or that it confers a small risk. Finally, overstatements regarding therapeutic prospects were found in 23% of the conclusions of all articles dealing with the mouse brain and related to ADHD. This percentage reaches 60% in articles published in high impact factor journals. Therefore, our observations were based on systematic searches and showed that two out of three types of data misrepresentation are frequent and spread in the media.

As are many scientists we are worried to observe huge gaps between biological observations and many firm conclusions stated in the media [Bubela et al., 2009]. This gap is observed in all fields of biology, including genomics [Evans et al., 2011], and “there is no reason to think that it is worst in the field of ADHD” [Gonon et al., 2011]. The originality of our research is that we have explored how this gap is generated by analyzing how specific topics are presented in the scientific literature and in the media. We believe that a deep understanding of the social mechanisms contributing to this gap is required to suggest appropriate corrective measures.

Finally, to go beyond controversies, we would like to point out why the lay public should be accurately informed that environmental factors play a central role in the development of ADHD. First, regarding parents of ADHD children, the genetic factors are often put forward to stop them feeling guilty. However, Dr. Eric Taylor disagrees: “In counseling parents, therefore, it is not desirable to convey a crudely biological notion of a genetic illness whose manifestation has nothing to do with environmental influences. To the contrary, many environmental associations with ADHD are known, and need to be enquired about in a full assessment” [Taylor, 2006].

Second, regarding the public at large, it is often assumed that a neurobiological understanding of mental illnesses contributes to reduce stigma. However, empirical studies regarding depression, schizophrenia, and alcohol dependence show that the opposite is true [Phelan et al., 2006; Hinshaw and Stier, 2008; Pescosolido et al., 2010]. “Holding a neurobiological conception of these disorders increased the likelihood of support for treatment but was generally unrelated to stigma. Where associated, the effect was to increase, not to decrease, community rejection” [Pescosolido et al., 2010]. Moreover, “clinicians need to be aware that focusing on genetics or brain dysfunction in order to decrease feelings of blame in the clinical encounter may have the unintended effect of increasing client and family feelings of hopelessness and permanence” [Pescosolido et al., 2010]. Although, we are not aware of similar studies regarding ADHD, similar trends are likely to occur regarding both ADHD and depression.

And third, the lay public also includes mental health policy makers. When ADHD is described as a genetic illness, prevention is dismissed. For instance, on the HealthCentral web site it is written: “ADHD is a neurobiological condition, however, the exact causes are not completely known but it is considered to be hereditary. There seems to be a higher risk if the mother smokes during pregnancy. However, beyond that there is no way to prevent ADHD.” Similarly, on the web site of the National Institutes of Health it is written: “ADHD may run in families … There is no proven way to prevent ADHD.” Therefore, if health policy makers are convinced that ADHD is a hereditary neurobiological condition, they will not consider the possibility that social measures might decrease ADHD prevalence. On the contrary, several environmental risk factors such as lead toxicity [Needleman et al., 1979], family-environment adversity factors [Biederman et al., 1995] and excessive TV watching between ages 1 and 3 [Christakis et al., 2004], can be decreased by appropriate measures. Likewise, premature babies and children born from teenager mothers are at higher risk of later development of psychiatric disorders, including ADHD [Black et al., 2002; Linnet et al., 2006; Gustafsson and Kallen, 2011]. The rate of preterm births ranges from 5% to 9% in European countries and reaches 12.7% in the USA [Goldenberg et al., 2008]. The number of births from 1,000 teenagers mothers ranges from 4 to 10 in continental European countries and reaches 42 in the USA (2007 data from the World Health Organization). These regional differences suggest that the rates of preterm birth and of birth from teenager mothers partly depend on social factors. Thus, these ADHD risk factors could be decreased by appropriate social policies.

In conclusion, because recent studies “demonstrate smaller and smaller molecular genetic main effects” [Sonuga-Barke, 2010], the relevance of genetic data towards ADHD prevention, diagnose and treatment appears weaker than it did in the 1990s. Moreover, a discourse to the lay public, which portrays ADHD as a genetic illness, has negative consequences. There is now a general agreement that environmental risk factors play a central role in ADHD etiology. We believe that taking them into account will decrease ADHD prevalence and improve ADHD diagnoses and treatment. It is our duty to say so in public.

Acknowledgements

  1. Top of page
  2. Dear Editor,
  3. Acknowledgements
  4. REFERENCES

This work was supported by the CNRS (UMR 5293), by the University of Bordeaux and by grants from the Région Aquitaine and from the Institut des Sciences de la Communication du CNRS.

REFERENCES

  1. Top of page
  2. Dear Editor,
  3. Acknowledgements
  4. REFERENCES