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Critics of ADHD as a valid entity have pointed out how subjective the diagnosis can be to interpretation about when a child’s activity level should be considered too high or an attention level too low. Accumulating research data has shown fairly conclusively at this point that one of the things that complicates the diagnosis of ADHD is that the behaviors that constitute it do not exist in a binary form (i.e. clearly distinct groups of people with normal and abnormal levels) but rather as a spectrum or continuum not unlike intelligence or blood pressure. I’ve written about this topic before on several PT blog posts here and here in addition to my book that addresses the overall question of trying to draw the line between traits and disorders.
What has been much less studied is the degree to which the causes and underlying neurobiology of ADHD behaviors also exist along a continuum versus there being somewhat separate things that contribute to attention and activity levels at moderate versus more extreme levels. This question has generated a debate within a small scientific community that has probably been too civil and esoteric to make headlines. Nevertheless, an examination of this topic was recently published in the Journal of the American Academy of Child and Adolescent Psychiatry.
The data come from a well-known study from England called the Avon Longitudinal Study of Parents and Children (ALSPAC). While the methodology is a bit complicated, the scientists basically checked over half a million genes from a sample of about 4,500 children to see which ones were associated with mild levels of hyperactivity and inattention. Mind you, they did not look at rare mutations that tend to have large effects but rather versions of genes, called single nucleotide polymorphisms or SNPs, that all of us carry to some degree. From this analysis they were able to calculate an overall “polygenetic risk score.” This score was then used to compare a different group of about 500 children with documented ADHD to a control group to see if these same common genetic variants that were related to trait levels of ADHD were also related to people with a full ADHD diagnosis.
The bottom line was that they were, although clearly these common genes were not the whole story for ADHD which is well-known also to be related to certain environmental factors (everything from parenting to lead exposure) as well as other types of genetic influences.
The authors concluded that their data support the hypothesis that the disorder of ADHD is best understood a part of a spectrum of normal trait variation.
This is just one study, but in a way is somewhat of a victory for both camps across the ADHD debate. Those who generally argue for the scientific validity of ADHD welcome this additional information which offers some real insight as to how something can be very real in the brain and in the genes but still evade detection as something a radiologist can point to on an MRI scan and say, “There’s the ADHD.” Critics of ADHD, however, can also use this study as support for the idea that viewing ADHD from a classic “brain disease” model perspective is problematic. The debate will surely continue, but the study is a nice illustration of how science can cut through a highly polarized and political topic to a conclusion that nobody, except me it seems sometimes, really likes.
@copyright by David Rettew, MD
David Rettew is author of Child Temperament: New Thinking About the Boundary Between Traits and Illness and a child psychiatrist in the psychiatry and pediatrics departments at the University of Vermont College of Medicine.
Follow him at @PediPsych and like PediPsych on Facebook.
