New Findings About Attention Deficit Hyperactivity Disorder
The NIEHS study suggests prenatal exposure to tobacco smoke increases a child’s chances for being diagnosed with Attention Deficit Hyperactivity Disorder (ADHD). Male children’s risks seems to increase by as much as 2 Ã?Â½ times over those not prenatally exposed to tobacco smoke and females seem to have a nearly 4 times higher chance than those not exposed to prenatal tobacco smoke. The study did not test for prenatal second-hand smoke exposure, only exposure through the mother. The same study also seems to link early lead exposure, even levels lower than what the United States government deems safe, can also increase their diagnostic chances by more than four times those not exposed. The study finally seems to indicate children who attend daycare or preschool have a higher risk of being reported and tested for ADHD than children who did not.
A recent overview of literature in the Official Journal for the American Academy of Pediatrics found the tricyclic antidepressant desipramine was as much as 68% effective in treating ADHD symptoms in adults, which is similar to earlier studies done on adolescents and children. This is a much higher rate than any of the other antidepressants currently used to treat ADHD, although not higher than the efficacy rate of stimulant medication. Therapy alone showed the lowest efficacy in treatment of the core ADHD symptoms, although it is one parents frequently choose as it also has the fewest perceived side-effects.
ADHD is one of the most commonly diagnosed childhood disorders and is rapidly becoming a massive burden on the healthcare system. It is estimated that 1.8 million children are diagnosed with ADHD and taking stimulant medication in the United Stated right now, but the exact cause of the disorder remains unclear. Children with ADHD are reported to be at risk for later drug abuse, conduct disorders and a host of academic and social problems. The NIEHS study seems to suggest two major environmental factors which cause a change in the way the human brain develops and processes information, which can then lead to an eventual psychiatric diagnosis of ADHD. However, other studies have reported a very strong genetic link to what causes ADHD. If one parent has ADHD there is as much as a 40% chance at least one child will also have ADHD.
In the recent NIEHS study, exposure to tobacco smoke after birth was not associated with an increased ADHD risk, showing that different toxins can impact the brain’s development at different times. It was assumed in the study that the mother did not somehow expose the fetus to lead during the pregnancy, but that lead exposure came after birth. The study also does not discuss the incidence of ADHD among the parents of the children as a possible factor influencing the eventual diagnosis, as it is possible that mothers with ADHD may have a higher rate of tobacco use than mothers not diagnosed. However, a previous study shows a link between increased hyperactivity in rats and nicotine exposure.
The NIEHS study was not clear whether ADHD (inattentive type) was included as part of the study at all as the subjects were required to be taking stimulant medication and have an ADHD diagnosis. Children who had one or the other were excluded from the study. ADD is the older diagnostic term, but is sometimes given as a separate diagnosis, as ADD (inattentive type). Children diagnosed with the inattentive type of ADHD are less frequently given stimulant medications and are infrequently a behavior problem as hyperactive children tend to be. Finally, some people are diagnosed with “combined type” which is a person who displays a number of symptoms from both ADHD and ADHD (inattentive type).
The NIEHS study, although flawed, gives some clues into what may have a hand in causing ADHD, but does little to address the possible genetic link. The second study offers some hope to parents who want to help their children, but are leery of stimulant medication.
The full NIEHS study is available in PDF at http://www.ehponline.org/members/2006/9478/9478.pdf
The initial desipramine stsudy can be found at http://ajp.psychiatryonline.org/cgi/content/abstract/153/9/1147