ebook_ADHD2019

10 Rohde, Buitelaar, Gerlach & Faraone loping brain and increase risk for ADHD. In addition to such biological adversity, studies have also implicated adverse psychosocial experiences as risk factors for the disorder. Examples of psychosocial stressors that affect children are marital distress, family dysfunction and low social class. In a population study conducted in Ontario, Canada, family dysfunction and low income predicted persistence and onset of one or more psychiatric disorders during a four-year follow-up period. Other potential risk factors for ADHD are low maternal education, low social class, and single parenthood. Several studies show that the mothers of ADHD children have more negative communication patterns, more conflict with their child and a greater intensity of anger than do control mothers and that families of ADHD children are more likely to have higher levels of chronic conflict, decrea- sed family cohesion, and exposure to parental psychopathology. However, most of the environmental factors might act more as unspecific triggers for mental health problems in general than specific environmental risk factors for ADHD. Com- paring to medical conditions, stress might be a trigger for gastritis for those with genetic predisposition for this disorder, while acting as a trigger for asthma for those with vulnerability for this disorder. MECHANISMS FOR THE ENVIRONMENTAL CAUSES OF ADHD Although we have been discussing genetic and environmental risk factors separa- tely, to fully understand the etiology of ADHD, we must consider how genes and environment work together to cause the disorder. Two mechanistic areas that are of clear theoretical importance are gene by environment interaction and epigene- tics. The DNA variants that increase risk for ADHD do not do so in a vacuum. They reside in cells where they build proteins in response to cellular signals. The environment may generate these signals. Gene by environment interaction occurs when mutant genes only cause disease in the presence of specific signals from the environment. For example, fetal anoxia creates oxidative stress which could trigger a cascade of events leading to abnormal brain development. Those with genetic variants that predispose to lower defenses of oxidative stress will be less able to de- fend against oxidative stress and more likely to suffer adverse impacts to the brain. Although there are many studies of gene by environment interaction in ADHD, none of have been consistently replicated to warrant discussion here. One key fin- ding comes from the ADHD GWAS study described in the prior section. There we reported that only 30% of ADHD’s heritability could be explained by the disor- ders polygenic architecture. Some of the other 70% will be accounted for by rare variants but it is likely that a good fraction of heritability will be explained by gene by environment interactions. Unfortunately, these are very difficult to study, as there are many relevant environmental risk factors to study.