Ongoing Patterns of Heterogeneity in ADHD Individuals

ADHD is one of the most well-known neurodevelopmental disorders that impacts 8-12% of children globally. Of those who are diagnosed, more than half continue to live with the symptoms that could negatively impact one’s well-being. These impacts range in many settings, from education and social interactions to parent-child relationships. There is significant evidence in many research studies that have supported the hypothesis of ADHD being a heterogeneous disorder, similar to ASD. Heterogeneity applies to many features, including risk factors, symptom expression, neurological impairments, etc. When considering the biological and environmental factors that are most prevalent, the brain’s neurological structure can be pinpointed as one cause of this heterogeneity, since the result would be a distinct cognitive and behavioral profile. 

Genetic variants (among the many alleles that make this a multifactorial condition) and risk factors right before and after pregnancy are among the most concerning in the development of symptoms. For one to be diagnosed with ADHD, their symptoms must feature age-inappropriate behavior of inattention, hyperactivity, or impulsivity. They can be put into three defined categories: predominantly inattentive, predominantly hyperactive/impulsive, or combined presentation of the prior traits. With that said, the diagnosis is not made from examining the risk factors that the person was previously exposed to or any biological aspects. In fact, there is still a common misunderstanding which questions whether specific factors are linked with specific symptom(s). A range of medical or psychiatric conditions is present in individuals with ADHD, showing that having one set of shared characteristics does not mean homogeneity. 

Impairments in the cognitive and neurological processes are an essential part of understanding the symptoms of ADHD. In accordance with the heterogeneity suggested prior, they include impairments in sustained attention, executive functioning (carrying out tasks), memory, and self-control, with all of these reported in varying frequencies but still prevalent. The degree to which these are present highly varies; some have none of these challenges. Additionally, the improper structure and functioning of the brain should also be examined. Specifically, the front lobe, thalamus, and striatum - main components of the pathway responsible for attention and cognitive processing - could lead to the emergence of ADHD, while the reduction of aDhd symptoms can be found in the proper functioning of the frontal cortex (personality) and other attention and processing loops. While these are just some proposals, the results of neuroimaging and neurophysiological studies indicate that the features present are fairly inconsistent. Even though the size of the frontal lobe was deemed to be one of the more important features, there is still a divide over whether the cortex was unilateral or bilateral; involved superior, inferior, or both areas; was made of white matter, gray matter, or both; and whether it resulted in an overall reduction in brain size or not. Furthermore, the studies which suggest the impairments in executive functioning to be directly caused by prefrontal cortex processes are rejected to be an overall view of the average ADHD individual because it was found that only 50-60% had an impairment in the sensitive executive function features. Like said before, the specific risk factors could explain this large heterogeneity in the neurology of ADHD. 

It’s not surprising that those whose relatives have ADHD-like behavior are more likely to develop the condition themselves. The heritability rate of ADHD falls within 60%-80% through a thorough understanding of the strong genetic factor(s) involved. A number of specific genes are found to be especially prevalent in studies investigating the genetic risk factors, such as dopamine receptor genes, norepinephrine receptor genes, serotonin receptor genes, and transporter genes. However, these findings are still inconsistent, with no definite pattern that can be used to identify ADHD based on the characteristics of these genes alone. Each of those gene types has more specifically defined gene types, and their association(s) with the characteristics listed in the name of ADHD is still somewhat of a mystery. Additionally, each of those genes was found to be only a small factor in contributing to a full-blown condition of the disorder. The influence of each specific gene as one proceeds into adulthood also changes and varies. That is, specific genes responsible for childhood development for ADHD may not be present to the same degree as, say, when that individual is in their 30s. New genes at that age could pop up and replace the old genes which were responsible at a younger age. All of this evidence supports the fact that ADHD is a developmentally complicated disorder with the continuous alternation of genetic features over the lifespan. 

Not discussing the environmental factors involved would result in an insufficient analysis of the risk factors associated with ADHD. The most frequent causes are factors right before and after birth, such as alcohol consumption and smoking by the mother, maternal stress, low birth weight and premature birth, and exposure to toxins. The latter is associated with being responsible for damaging the neural networks of the child. Likewise, damage to the brain from injury is also a risk factor. On the other hand, psychosocial features - such as child/mother hostility, low-income households, etc. - are possibly equally likely to be associated with ADHD. The biggest question with respect to these environmental factors is whether the factors are directly causal or simply the result of ADHD. The studies out there show a mix of both. It is plausible that the genetic and environmental factors work hand-in-hand in the development of ADHD.