I am deeply saddened by, and very annoyed at, the way that society is medicating children for this so-called disorder ADHD. It is a great seller of drugs! Here’s a recent blog from Mad in America on this issue.
Welcome! This blog presents a psychological understanding of the diagnostic category “Attention Deficit Hyperactivity Disorder” (ADHD). Over the past decades, professionals have been informing the public about the neurobiological causes of the behaviors, and the necessity to medicate and stringently manage those who have been afflicted. This blog critiques those claims.
While biological determinist claims may continue to prosper there is increasing concern that we are positing the existence of a medical problem when there are no biological markers or dysfunctions that reliably correspond with the behavioral criteria.
Over the coming weeks, I will also present an alternative intervention that develops self-management in individuals who have been diagnosed as ADHD. This intervention is designed to replace traditional treatments which have been yielding very poor longer-term benefits.
The Fragile Pillars of Biological Causality
Let’s examine the foundation of ADHD biological determinism. This view speculates that ADHD represents a neurological delay that forever keeps a person from showing competency in self-management. Three research finding (or, as I call them, “pillars”) form the basis of this position.
1) ADHD runs in families
Often identical twins are the same when it comes to ADHD.
There are studies which suggest that molecular biology increases the likelihood of ADHD.
2) The brain biology of groups of people with ADHD differs from those without ADHD
3) Medicine (which alters biology) ameliorates ADHD
So let’s examine each of these “pillars.”
1) ADHD is genetic
There are individuals with ADHD who do not have the molecular biology associated with ADHD. There are individuals without ADHD who have the genetic material associated with ADHD.
The occurrence of these false positives and negatives indicates that genetics is not the cause of ADHD.
From a psychological viewpoint, we expect that an ADHD (and many other patterns of behavior) will run in families. People in families tend to have similar bodies and experiences, so they are likely to learn in similar ways. This (of course) amplifies with identical twins.
Many behaviors (including poverty) and various psychiatric diagnoses run in families. However, similarity amongst related individuals tells us nothing about how different these people might become with the introduction of different environments.
2) Brain biology is different for those with ADHD
The finding that ADHD brains (on average) are different shows a correlation between people who respond with ADHD behaviors and certain kinds of biological patterns. Cause and consequence are not determined.
Yes, endogenous factors may increase the likelihood of developing ADHD behavior. When particular kinds of problems and impairments occur (which make it difficult for people to meet expectations) ADHD behaviors can become prevalent.
However, doing ADHD behavior (over time) may also change a person’s biological development just like what happens with muscle mass when people fail to exercise. This outcome is illustrated by Walsh et al. (2014) who show that exposure to environmental stress reduces the size of the cerebellum.
It is evident in Maguire et al. (2000) study which shows that the spatial cortex of cab drivers will show greater develop as a consequence of navigating city streets. And it is made clear in Gaser and Schlaug’s (2003) study which shows that the brain’s “planum temporale” develops as a function of playing a musical instrument.
3) Medicine is effective
We do not know the etiology a problem just because medicine ameliorates the behaviors. For example, alcohol might help a person to become more sociable, but that does not tell us why the person was not sociable. Treatments do not tell us about causation.
An Alternative Way to Conceptualize ADHD
There are no dysfunctions of any kind that can be used to make the ADHD diagnosis. ADHD behaviors occur in particular situations and circumstances and increase in frequency in relation to what happens.
Rather than delayed behavior, ADHD behaviors are ways to cope (i.e., reinforced behavior) and, like other behavioral responses, they yield advantages and side effects.
In this alternative view, the label “ADHD” is affixed when people do particular avoidant and intrusive behaviors more often than others. The behaviors are more likely when individuals are responding to the adversity (often responding to the agendas imposed by others) and least likely when individuals are doing what they initiate and enjoy (situations associated with pleasure and success).
What is the Role of Biology in this Formulation of ADHD?
Biology changes the probably of what is learned (e.g., if a person is agile, he is more likely to enjoy playing sports and participate frequently, and if he is clumsy, the opposite is likely).
However, depending upon life experiences, people with similar biology may learn to live in the world in different ways (e.g., some very agile people might learn to dislike sports). This is why early occurring biology is often a poor predictor of subsequent patterns of behavior (e.g., psychiatric diagnoses). And if people live in the world in a particular way, their biology is likely to reflect the way they live and learn.
Conclusion:
People with a particular kind of biology may have a slightly greater probability of an ADHD diagnosis. However, experiences along the way can alter the course of development even with this temporal origin.
Particular genes and various early occurring problems (e.g., negative infant temperament, high activity levels, motor coordination difficulties, health problems, etc.) can increase the likelihood of an ADHD diagnosis, but these problems do not seal an individual’s fate. People with similar starting points can have different psychological and biological developmental trajectories.
References:
Gaser, C., and G. Schlaug. “Brain Structures Differ between Musicians and Non-Musicians.” The Journal of Neuroscience 23, no. 27 (2003): 9240–45.
Maguire, E. A., D. G. Gadian, I. S. Johnsrude, C. D. Good, J. Ashburner, R. S. Frackowiak, and C. D. Frith. “Navigation-Related Structural Changes in the Hippocampi of Taxi Drivers.” Proceedings of the National Academy of Sciences, USA 97 (2000): 4398–403.
Walsh, N., Dalgleish, T., Lombardo, M., Dunn, V., et al; General and specific effects of early-life psychosocial adversities on adolescent grey matter volume. Neuroimage: Clinical. Volume 4, 2014, Pages 308-318. http://dx.doi.org/10.1016/j.nicl.2014.01.001′
