ADHD and brain drainers
27 May 2014. Attention deficit hyperactivity disorder (ADHD) is the most common behavioral disorder of childhood, and the prevalence among school children may be as high as 10%. Children with ADHD have a decreased attention span, they have difficulty concentrating, they are more impulsive and often hyperactive. The symptoms change with age, and ADHD in adults is associated with academic underachievement, employment problems, decreased income as well as unstable personal relationships and injury risks. ADHD is a major public health problem. A review by US researchers examines why ADHD has become so common in modern society.
So far, the etiology and pathogenesis of ADHD are poorly understood. Nonetheless, toxic chemicals play a role, the most obvious culprits being prenatal exposure to cigarette smoke and alcohol, and postnatal exposure to lead. However, the detailed dose-response associations are still unclear. The time and duration of exposure are important, though difficult to document, as the causative exposures may have occurred during early life, perhaps several years before diagnosis. Several studies suggest that exposure to organophosphate pesticides, especially prenatally, may lead to ADHD development. Another recent review emphasized manganese, organochlorine pesticides (such as DDT), and PCBs as potential causes of ADHD, but again stressed the uncertainties and the need for better exposure assessment in future research.
Most research so far has focused on single risk factors and not accounted for exposures to other chemical brain drainers that might have influenced the findings. Given that we are all exposed to a cocktail of many different chemicals, many of which may be toxic to brain development, a comprehensive exposure assessment would seem necessary. This has just been attempted in a prospective study in children from Cincinnati, where behavioral problems at age 4-5 years were related to the concentrations of 52 chemicals in blood and urine samples from the mothers during pregnancy. Some suggestive links were discovered, but are difficult to interpret based on what we know so far.
An additional problem is that genetic predisposition may make some children much more susceptible to brain-toxic chemicals. For example, a common mutation in the alcohol dehydrogenase gene is associated with a greater risk of developing ADHD behaviors. For pesticides, mutations in the paraoxonase gene also seem to play a role in determining whether a child may be affected by an exposure. This does not mean that ADHD should be considered an inherited disease. However, the genotype will likely affect the vulnerability to brain drainer exposure, so that some children are affected to a much greater extent than others. Most studies have not considered such interactions, which may be one of the main reasons for variable or non-significant findings.
The bottom line? ADHD is a diagnostic term that likely reflects a multitude of different pathologies and etiologies. At this point, we can be fairly certain that maternal alcohol intake and smoking, as well as childhood lead exposure can contribute to ADHD development. We can also be fairly certain that other brain drainers contribute, but we don’t know the extent to which this happens. That does not mean that brain-toxic chemicals can be disregarded. Given that ADHD is a chronic condition, perhaps lasting a life-time, ADHD is another reason for us to reduce exposures to brain drainers.