The Origins of ADD

Characterized by poor attention skills, hyperactivity, and an inability to control impulses, Attention Deficit Disorder (ADD) impacts an estimated seven percent of the population (1)(2).  It is thought that ADD occurs due to missing neural connections and a lack of blood vessels in the pre-frontal cortex (2).  There has been research to suggest that the causes of ADD are due to a lack of dopamine receptors and transporters (2).  In recent years, there has been an increase in the number of children diagnosed as ADD (2).  Because of this, there has been an increase in research with the goal of determining the cause of ADD.  With this, several theories have emerged to explain the reasons behind ADD.  This paper is a critical examination of these possible origins.
 Research suggests that there is a genetic component to ADD (1)(2)(3).  Twenty five percent of children with ADD also have close relatives with ADD.  By contrast, this only applies to 5 percent of the general population (3).  One study suggested that up to 80 percent of ADD can be linked to genetic factors (4).  Currently, there is research being conducted to ascertain which genes are responsible for ADD (5).  So far, the genes that have been isolated are associated with dopamine receptors.  Most scientists who research ADD hypothesize that it is not a single gene that causes ADD but multiple ones.  The genetic explanation for ADD is logical because of the high correlation between parents and children with ADD.  That being said, there are probably other factors that can influence this disorder.

Some research suggests that ADD is a result of brain injury.  In some children who have suffered traumatic brain injuries, they have later shown symptoms of ADD (3).  Lead poisoning is also thought to be a cause of brain damage (3).  Some studies found that children who have been exposed to lead are more likely to demonstrate ADD symptoms.  Children may also experience brain damage in the womb.  One study discovered that mothers who smoke when they are pregnant are more likely to have children with ADD.  They hypothesized that this is because smoking causes there to be a lack of oxygen supplied to the baby which impacts their brain development (6).  However, it has been shown that people with ADD are also more prone to addictions (2).  Because of this mothers who smoke while they are pregnant may also be ADD.  It is therefore difficult to separate how much of the correlation between smoking mothers and children with ADD is attributed to genetics or to the fact that the mother smoked while pregnant. 

Some experts argue that parenting factors are responsible for the development of ADD.  This is based on the fact that ADD is thought to be caused from a lack of neural connections.  These connections are particularly fragile when they are being formed when the child is an infant.  Some argue that the amount of nurturing that the child receives promotes the development of these connections.  Therefore, children who do not receive the attention required for these connections to form when they are young are more likely to develop ADD when they are older (2).  It is likely that environmental factors can exacerbate ADD, but most agree that ADD cannot “arise purely from social factors or child-rearing methods” (3). 

Others argue that ADD can be attributed to food additives and refined sugar in our diet.  Approximately 2 to 3 percent of children with ADD also have hyperactive reactions to food dyes (1).  A 1982 study performed by the National Institutes of Heath explored this possibility that refined sugar was responsible for ADD.  It was found that restricting the diet of ADD patients caused five percent of the participants to show less severe symptoms (3).  However another study found contrasting results.  In this study, children with ADD were given sugar some days and a sugar substitute on other days.  Parents, teachers, and children were unaware of which substance was being used on which day.  The researchers found that there was no significant impact of sugar on the children’s behavior or ability to stay focused to learn (3).  The ambiguities among these suggest that nutrition and diet is not a primary cause of ADD.  Although it is possible that it can exacerbate symptoms, it is probably not the leading origin.

This paper has presented several possible causes of ADD.  Because of the wide ranging possibilities of origins, it is difficult to pin down which explanation is the most logical.  Thus far, it appears that there is a strong genetic component that causes ADD.  While the other factors such as child-rearing styles, brain injuries, and food additives have the potential to exacerbate ADD symptoms, there is little hard evidence that these factors alone can cause ADD.  In reality, it is probably a combination of several of these players that leads to ADD.  That being said, I have to wonder, how important is it that we find the “real” reason behind ADD?  Is ADD really a disorder, or is it merely an expression of different organization of the brain.  Although it is interesting to examine the differences in peoples’ brains, it is important that we question the implications of the results of this research.  Hopefully the results from ADD research will provide strategies for those with ADD to cope in a world that is so often unforgiving of those with disabilities.

(1)Copps, Stephen.  Attention Deficit Disorder: Where We’ve Been, Where We Are, and
         Where We’re Going.  Attention Deficit Disorder Association.  <www.add.org>.

(2) Maté, Garbor.  Scattered: How Attention Deficit Disorder Originates and What you
         Can do About it.  New York: Dutton, 1999.

(3) National Institute of Mental Health.  Attention Hyperactivity Disorder. 
        < http://www.nimh.nih.gov/publicat/adhd.cfm>.

(4) Schwab Learninghttp://www.schwablearning.org/pdfs/2200_7-barktran.pdf?date=4-12-05

(5) Swanson JM, Flodman P, Kennedy J, et al. "Dopamine Genes and ADHD." Neurosci
         Biobehav Rev. 2000 Jan;24(1):21-5.
       
(6)  Kotimaa AJ, Moilanen I, Taanila A, et al. ,"Maternal smoking and hyperactivity in 8-year-old children". 2003, J Am Acad Child Adol Psychiatry Jul;42(7):826-33