Everyone knows not to feed children sugar before bed, but new theories suggest that chronic sugar intake can cause even more hyperactivity than previously thought. Characterized by inattention, inability to focus, and impulsiveness, attention deficit hyperactivity disorder is prevalent in both adults and children. As the number of people with ADHD in America has risen, so has sugar consumption. Scientists are beginning to suspect that chronic sugar intake may alter the mesolimbic dopamine pathways that are affected in those with ADHD.
In the 1980s and 1990s, scientists performed numerous studies investigating the relationship between sugar intake and ADHD. Today it is understood that since sugar activates dopamine release via taste receptors in the mouth, even artificial sweeteners can impair the mesolimbic dopamine system. Therefore, scientists are returning to the study of sugar’s effects on dopamine signaling with a more precise approach.
Scientists have long studied the causes of ADHD and have attributed its presence to a genetic defect, such as polymorphisms of the genes that code for dopamine neurotransmission. Increasing evidence shows that ADHD does indeed involve changes in dopamine signaling. Yet, to date, the small number of identified genetic linkages accounts only for a portion of ADHD cases. This is one more reason scientists have returned to the search for other possible causes of ADHD.
While the cause of ADHD is not certain, most research suggests that it is associated with impairment in dopamine signaling. Dopamine receptor activity is involved in the proper functioning of control mechanisms in the area of the cortex associated with rewards. In the absence of sufficient dopamine receptor signaling, the inhibition generated by the frontal control mechanisms is reduced. The result is impulsivity and irregular attention and behavior.
Such impairment arises from the excess dopamine which can result from increased sugar intake. Upon eating, the sweet taste receptors in the mouth stimulate dopamine release in the brain. The receptors become habituated to the dopamine because of their prolonged exposure to it and proceed to respond to the dopamine with less intensity. The desensitization is seen most clearly in experiments involving rats that eat progressively higher amounts sugar, and whose dopamine response remains the same nonetheless. As a result of desensitization, the body needs even more sugar, and more dopamine, to stimulate a favorable response. People with drug addiction and obesity have the same dopamine signaling impairment. Thus, the pathway becomes a cycle.
Scientists’ knowledge about ADHD correlates with the changes that increased sugar intake can cause in the body. Adults with ADHD show fewer dopamine receptors in the part of the cortex associated with reward behavior. Additionally, reduced activity in the prefrontal cortex that results in the absence of cortical control mechanisms is observed in ADHD patients. Children with ADHD show lower levels on dopamine in cerebral spinal fluid. These overlapping findings reaffirm that chronic sugar intake may be triggering the physiological symptoms that mark ADHD.
Researchers have further confirmed this theory in the patterns of the spread of ADHD. They cite the correlation of the spread of excessive sugar consumption and the prevalence of ADHD. Also, both ADHD and chronic sugar intake are associated with obesity. Some propose that perhaps it is sugar intake that drives both ADHD and obesity, which is why the two often appear together.
The connection between sugar intake and ADHD requires further experimental and clinical investigation. Researches have begun to study the subtle differences between the effects of glucose and fructose but are still concretizing their findings. Additionally, while the evidence for the correlation is clear in animals, it would be worthwhile for scientists to pursue similar studies in humans. Further studies may include separating children and adults to examine whether sugar has more severe effects on one group, especially since children below age seven are believed to be most disposed toward developing ADHD. It is also important to probe if there is a lower prevalence of ADHD in individuals with lower sugar intake. The theory of sugar intake as a cause of ADHD seems promising; however, there remains work to be done in developing experimental evidence to substantiate it.
A strong case for the role of sugar intake an ADHD would have profound implications for treatments and public health campaigns. Long-term pharmacological treatments can have adverse side effects and can be a financial burden. Understanding the role of a healthy diet in the prevention and treatment of ADHD can one day offer a cheaper alternative. Furthermore, in a time where measures toward healthy diets are becoming increasingly popular, finding a link between sugar intake and ADHD would be an important push in the right direction. In the case of sugar and ADHD, diet does not simply influence the body, but it can change how a person thinks. Should this theory continue to gain support, it may be proof that mind-body connections are not far off. A healthier body truly does create space for a healthier brain.