At the UnRitalin Solution, we believe that the onset of ADHD is caused by the complex interaction between a genetic predisposition and environmental factors. Although our destinies are not determined by the limitations imposed by our genes, it helps to take a look at the genetic influences of ADHD and its co-morbid disorders. The presence of some of these genes can explain the dominance of certain ADHD symptoms over the others. Try not to be too overwhelmed by the terminology – the main point of this article is to show the intricate relationship between ADHD, genes, and how these can influence some treatment outcomes.

DAT1 Gene

The dopamine transporter gene or DAT1 is a mutated form of the dopamine transporter protein that carries the neurotransmitter dopamine to and from neurons. If you remember, dopamine is the neurotransmitter responsible for pleasure, motivation, and movement. It is also the target of ADHD medications like Ritalin. The dopamine transport protein allows for the normal movement of dopamine among neurons, but DAT 1 tends to make it move the opposite direction at high speeds, affecting the distribution of dopamine and resulting in ADHD symptoms.

MAOA Gene

The moanamine oxidase enzyme (MAOA) is a unique ADHD-related gene because it is located on the X-chromosome – the sex-linked chromosome. The presence of this gene can probably explain the gender differences in ADHD types – boys typically exhibit hyperactive symptoms whereas girls experience inattention and are more likely to develop anxiety disorders. Research on mice suggests that certain mutations on the MAOA gene may be linked to higher anxiety levels. A small study shows that a deficiency in this gene is also related to aggressive and impulsive behaviors.

NET

Yet another gene that can account for gender differences in ADHD, NET or the norepinephrine transporter protein often turns up in higher frequencies among women. Norepinephrine is an important neurotransmitter that activates the fight-or-flight response, and deficiencies in this chemical are often spotted in individuals with ADHD. Some studies show that individuals with ADHD who have the NET gene have higher rates of eating disorders than the rest of the population; in fact, a certain form of this gene seems to be related to the risk of developing anorexia.

Fatty acid desaturase genes

Omega-3 fatty acids are critical to the proper functioning of the brain and maintaining the structure of neurons. There are two long-chain omega-3 fats that have this specific purpose – eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Alpha linolenic acid (ALA) is the “mother” of omega-3 fats that become converted into EPA and DHA in the body using a substance called desaturase enzymes. When the desaturase enzymes function properly, the body can make use of omega-3 fatty acids efficiently. However, there are some genes and external factors (like eating other types of fat) that can impair the function of desaturase enzymes and slow down the conversion process. In some cases, these genes can even prevent the body’s use of omega-3 fats. The presence of fatty acid desaturase genes can explain why omega-3 supplementation does not reduce ADHD symptoms in some individuals.

CREM Gene

One commonly overlooked symptom of ADHD is sleep disturbances. Children and adults with ADHD have a harder time falling asleep, staying asleep, and waking up than those without the disorder. They are also more likely to have abnormal sleep patterns. Experts believe that the mutations in the CREM gene may be responsible for this. The CREM gene regulates the production of the sleep hormone melatonin. Normally, low levels of melatonin are produced in the daytime, while high levels of melatonin are produced at night, which brings about the feeling of sleepiness. However, problems with the CREM gene can cause certain changes, such as disrupted sleep patterns, high melatonin production in the daytime, and excessive activity at night.

Researchers have also found evidence that some of these ADHD genes might work together to bring about certain symptoms. For instance, some variations in the DAT gene and the MAOA gene may be associated to the presence of anxiety disorders with ADHD.

In this blog, I have reviewed the main genes that prepare the ground for ADHD. However, genes are just the loaded gun. A child won’t develop ADHD until someone press the trigger, and the triggers for gene expressions are environmental factors. By changing those factors you can reduce the risk of developing ADHD or reduce ADHD symptoms expression. Check out our Unritalin Solution to view an organized map of all the environmental factors you can change.