Environmental Variable

Although the general public believes that certain diets cause hyperactivity, this is not the conclusion of the professional community. An often heard belief is that sugar has an adverse effect on ADHD symptoms. Although anecdotal reports are plentiful, and some correlational studies have found a small relationship between sugar and ADHD, the experimental research has concluded that sugar has no effect on ADHD symptoms. An important note comes from a study in which mothers were either led to believe that their children were given Kool-Aid with sugar or with aspartame, in fact, none of the children were given sugar and drank Kool-Aid with aspartame. Following the drink, the children and their mothers played and worked together. The mothers who thought their children were given the sugar sweetened Kool-Aid rated them as more hyperactive and were more critical and talked to their children more during their interactions than did those who believed that their children had drank aspartame sweetened Kool-Aid. The importance of these findings is that beliefs can be powerful in their potential influence--in this case, how the child with ADHD is seen and treated.

The most celebrated proponent of the effects of diet on ADHD was Feingold, a physician-researcher, who published Why Your Child is Hyperactive in 1975. Feingold asserted that foods containing artificial dyes and flavors, preservatives and naturally occurring salicylates, such as those found in tomatoes, cucumbers, prunes, and apricots, were related to hyperactivity. He further asserted that the behavior of 25-50% of children diagnosed as hyperactive-learning disabled improved when these substances were eliminated from their diet. Furthermore, Feingold claimed that when these children were returned to a diet that contained some of these substances, their behavior worsened and persisted for several days thereafter.

The first study examining these claims found that teachers, but not parents, reported that the behavior of children with ADHD improved on the Feingold diet. Further research found that the results were at best ambiguous but overall did not support Feingold's claims (Conners, 1980; Gross, Tofanelli, Butzirus, & Snodgrass, 1987; Harley & Matthews, 1980; Spring et al., 1987). Thus, although foods cannot be said to be a primary cause of ADHD, it must be noted that approximately 5% of children with ADHD do benefit from special diets. These children tend to be very young and those who are allergic to certain foods. In sum, diet is not a significant contributor to ADHD symptom severity, and where such data does exist, it is for a very small and young sub-sample of children who also suffer from allergies.

An interesting observation is that there is a relationship between certain mental health problems and fatty acids. So, the inevitable question is whether there is a relationship between fatty acids and ADHD.

Let’s start with a very brief overview of fats that are made up of fatty acids. Nature provides us with three classes of fatty acids. First are saturated fatty acids; second are monounsaturated fatty acids; and third are polyunsaturated fatty acids. A fourth class is the trans-fatty acids that are chemically modified; these are the unsaturated fatty acids and typically are not found in nature. When ingested, they do not function as well as those found in nature.

The body needs two essential fatty acids: linolenic acid (omega-6) and alpha-linolenic acid (omega-3). Although the body needs these fatty acids, it cannot produce them. Therefore, they are obtained through diet. Finally, there are the conditionally essential fatty acids that the body does produce, but not always--for a number of reasons. These too need to be obtained through diet.

Deficiency in fatty acids produces the following symptoms: eczema, dry skin, asthma, thirst, frequent urination, and allergies. Interestingly, these symptoms are common in children suffering from ADHD. There is also a gender difference: males need more fatty acids than females. This suggests that we should see a higher rated of ADHD in males than in females. This is in fact borne out by the literature: there is a 3:1 male-to-female ratio in ADHD.

A study by Sinn and Bryan (2007) shed some light on the use of fatty acids and the treatment of ADHD. The study involved one hundred sixty-seven 7-12 year old children--128 boys and 38 girls. Based on parental completion of the Conner’s ADHD Rating Scale, those who were in the top 2.5% were asked to participate provided that, in the past 3 months, they had not used stimulant medication or any form of omega-3 supplement. The study was methodologically sound using a placebo-controlled design; the participants were randomly assigned to 1 of 3 groups. Group A received an omega-3 fatty acid supplement and a daily multi-vitamin pill. Group B was exposed to the same treatment as Group A minus the multi-vitamin supplement. Finally, Group C received a placebo, palm oil, that looked identical to the supplement received by Groups A and B. The Conner’s scale was re-administered at week 15. At week 16, the members of Group C, without the parents’ awareness, were provided the active fatty acid supplement for the next 15 weeks. Group A and B continued with their intervention. The Conner’s scale was re-administered for the final time at week 30.

The results indicated that Groups A and B, those receiving the fatty acid supplement during the first 15 weeks, showed significant improvement over Group B (receiving the placebo). The improvements were in inattentive symptoms, hyperactive-impulsive symptoms, cognitive problems, and oppositional behavior. No significant differences were found in social problems and anxiety. Finally, the addition of the multi-vitamin did not have an impact on the ADHD symptoms. The switching of Group C from a placebo to the fatty acid supplement showed changes in behavior similar to those seen in Group A and B. At the end of 30 weeks, the children in Group A and B continued to show improvement so that the original modest magnitude of the change had become similar to that reported as a result of psychoactive medication. Unfortunately, the evaluation by the teachers did not report changes similar to those reported by the parents, either at 15 weeks or at 30 weeks.

In summary, although promising as a relatively safe alternative to psychoactive medication, fatty acid supplements need to be tested further to determine their efficacy as a reliable treatment for ADHD. Given this treatment, as with all other treatments of this disorder, children will continue to display behaviors that will need additional interventions.

Lead is a metal that adversely impacts humans. Lead is found in flaking paint, especially in older homes when lead was added to paint, older water pipes, dust, soil, and leaded gasoline. Even exposure to low levels of lead, over an extended period of time has an adverse effect on humans. Understandably, studies of the effects of lead in humans are necessarily correlational. These studies examine lead levels in the blood and, on occasion, in the dentine of children's deciduous ("baby") teeth. Overall, these studies have not found a relationship between lead levels and ADHD. Occasionally, studies designed to take methodological issues into consideration have identified a small relationship.

For example, one study found that dentine lead levels at 6 to 8 years of age correlated with inattention when the child was 12 to 13 years of age (Fergusson, Horwood, & Lynskey, 1993). Studies have confirmed that although children with ADHD have higher levels of lead in their bodies than do control participants, these levels are not significantly higher. At best, the amount of variance accounted for by lead poisoning in children with ADHD is no more than 4% (Barkley, 1996).

In summary, although there is a relationship between lead levels and ADHD symptoms, the relationship is at best a weak one.

Although it would appear that dysfunctional families would produce children with ADHD, this is not the case. Both dysfunctional and functional families have children with ADHD. Currently, the research indicates that approximately 10% - 15% of the variance is accounted for by family factors (Barkley, 1996).

Obviously, the family environment does contribute to the development of ADHD. Four factors are influenced by the family environment. Let us first examine the situation in which a child born with a predisposition to ADHD is born into a normal family environment to see how the interactions between child and parents may lead to the development of ADHD. In these families, the family difficulties may be due to the difficult-to-manage child. In other words, the family problems are the consequence of the interactions between the difficult child and that child's normal parents (Mash & Johnston, 1990). To determine whether this hypothesis had any merit, families were observed prior to and following the prescription of stimulant medication for their children. The result was that as the ADHD symptomatology decreased with the medication, the rate of conflict in these families also decreased (Barkley, 1988a; Humpries, Kinsbourne, & Swanson, 1978).

Another approach to examining the development of ADHD is to examine particular parenting practices. For example, insensitive and intervening early care-giving practices, found especially among some lower SES families, have been found to be contributors to the development of ADHD (Bauermeister, Algeria, Bird, Rubio-Stipec, & Canino, 1992; Jacobvitz & Sroufe, 1987).

For example, children who were diagnosed at age 3 years with ADHD and again when they were 6 years of age were found in families that had experienced greater stress. Moreover, the stability of the problems in such families can be predicted by an unfavorable mother-child relationship. Although this intrusive and controlling parenting style can exacerbate the predisposition for ADHD, it is also true that such an exacerbation can occur in the classroom. For example, a teacher's impatience may influence the attentiveness of the child with ADHD. In addition, the structure of the classroom may contribute to such exacerbation and academic performance.

The consistency of parenting techniques is also a fruitful way of understanding the development of ADHD symptomatology. For example, school-age children with hyperactivity have mothers who are not very consistent in their parenting techniques and are more impatient and call on the authority of power to enforce behavior compliance. Such problems persist into adolescence and escalate if the adolescent is oppositional.

Another approach to examining family influences is the relationship between parenting style and child predisposition to ADHD. The hypothesis is that children born with a predisposition to ADHD develop the associated symptoms when born to a dysfunctional family that involves much conflict. It is this interaction, between the biological predisposition and the confrontational family style, which shapes the hyperactivity-impulsivity to clinical levels. In this family environment, the child's temperament plays an important role. This interaction is referred to as the ‘goodness of fit’ between the child's temperament and the parenting style.

For example, a parent who over-stimulates a child born with an overactive temperamental style may eventually lead to the development of ADHD symptoms. As discussed earlier, there is a relationship between a parent who was diagnosed with ADHD and that person's offspring. It is possible that such over-stimulatory activity on the parent's part may be due to ADHD symptoms. This line of reasoning, then, suggests that the parenting style may disrupt important early parent-child interactions.

Another approach to examining the influence of various factors on the development of ADHD is to compare familial factors with biological ones. In a study assessing the impact of biological and psychosocial risk factors on ADHD symptom severity, Freitag et al. (2012) examined the pre- and perinatal biological risk factors with those of lifetime psychosocial risk factors and parental ADHD. The researchers reported that the risk factors for inattention were strongly influenced by psychosocial factors, whereas hyperactive-impulsive symptoms were primarily influenced by biological risk factors.

In conclusion, although family practices are not the cause of ADHD, family practices are crucial in exacerbating a predisposition and determining the outcome of ADHD. What is important about these findings is that family factors are central to ADHD; they are the context within which this disorder develops. What is unclear, even after thousands of studies, is the direction of causality in the development of ADHD.