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Heritability of ADHD

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The evidence regarding the presence of a genetic component as a cause of ADHD is especially prominent. Family, twin, and adoption studies are prime examples of that evidence, with a proven heritability rate of ADHD over 74%. Since there is such a high heritability risk, the hunt for highly susceptible genes is important to the path of finding ways to limit the risks of developing the disorder. When examining research studying the impact of different DNA variants, they turned out to be insignificant. On the other hand, studies investigating the association of various genomes have indicated several loci (locations of the genes) where their impact on ADHD is statistically significant. Additionally, a polygenic component may account for around ⅓ of the reason for the genetic heritability. This includes many genes, each with a small effect but amplified together. By studying the variants in these specific genes, we can learn about the significance of gene insertions or deletions, resulting in the discovery of new biological pathways that can be targeted for treatment. 



A study involving a large number of ADHD individuals and their siblings between the ages of 5-17 discovered a 9 times increase in likelihood for developing the disorder compared to individuals without ADHD. This occurrence is most likely the result of genetic factors rather than environmental factors. The number of 74% mentioned earlier comes from twin studies, which revealed the heritability among twins was that particular number. Another similar study even saw a rate of around 80%, regardless of gender. A possible range that could fit the trend would be somewhere between 77 - 88%, consistent with the larger studies of ADHD heritability. Evidence from these studies simultaneously suggests that the diagnosis of the disorder should be evaluated based on an extreme distribution of its symptoms within individuals and strong etiological factors that can be accounted for. When asking others besides the individual themselves to identify symptoms, it resulted in a larger heritability rate than when asking individuals to evaluate themselves. Therefore, self-reporting ADHD symptoms tends to be less accurate than when others report them.  While twin studies regarding adolescents and children have a high heritability rate, one study involving adults only had rates of around 30-40%. However, this study was most likely an exception, as other studies reported higher rates of more than 70%. The fact that the heritability of ADHD remains stable is most likely consistent with these results. 



Many of these twin studies have emphasized the duality of stable and dynamic genetic factors influencing ADHD over the lifespan. Indeed, the disorder is also associated with both stable and dynamic processes. Additionally, the stable process informs us that the childhood form of the specific genes highly influences their continuation, while the dynamic portion indicates that the set of genetic variants accounting for ADHD is different from those accounting for the continuation of the disorder. There exists a general genetic factor that influences the disorder and the spectrum of its conditions, which could simplify things, along with a set of latent (excess) shared genetic factors. Assessing the contribution of genetic variants estimated the SNP (single nucleotide polymorphism) heritability to be anywhere from 18% to 38% regarding the psychopathology dimensions of the disorder. These studies also support the existence of spectrum-specific genetic factors, such as one specifically accounting for the externalization of ADHD.

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