Candidate pathways for any condition may be identified based on effectiveness of pharmacological agents and their target molecules. In ADHD Ritalin and Concerta (methylphenidate) are used as first line treatments. These medications mainly act on dopamine (DA) and noradrenaline (NA) systems; the neurotransmitter, serotonin, is not their direct target. Interestingly, 30 percent of ADHD cases are, ‘non-responders’ to first line treatment. Moreover, among responders, an improvement in ADHD symptoms is observed in 50 percent of cases. This being so, researchers have started to investigate whether a chronic deficit of serotonin (5-HT) could possibly trigger symptoms of ADHD.
Response inhibition, that is the ability to suppress inappropriate action, is considered to be a core deficit in ADHD. Interestingly, serotonin has been shown to influence behavioural inhibition and aversion in neurocognitive models for ADHD. It has been previously reported that a decrease in 5-HT levels can feature among hyperactive and ADHD children, particularly in children diagnosed with co-morbid conduct disorder. Interestingly, selective serotonin reuptake inhibitors (SSRI’s) and tri-cyclic antidepressants which act on the 5-HT system have already shown an ability to reduce ADHD symptoms by a further 25 percent. In reading the foregoing sentence, it is important that you appreciate that I am not intending to encourage use of antidepressant medication for ADHD, but to highlight that the neurotransmitter serotonin appears to play a role in the aetiology of ADHD.
Published studies have measured 5-HT or its metabolite levels in the peripheral system, under the assumption that in healthy individuals, the peripheral system reflects central nervous system activity. For example, the observations that blood 5-HT levels are decreased in hyperactive children has led to the hypothesis that serotonin is involved in the aetiology of ADHD. However, not all studies reflect involvement of serotonin in ADHD, thus, resulting in mixed findings. One reason proposed as to why there is ambiguity of findings is considered to be the age of patients when assessed, given that prior and during adolescence developmental changes are most heightened. This being the case, it may be best to undertake assessment with adults diagnosed with ADHD, to provide a more accurate understanding of 5-HT levels in the aetiology of ADHD.
In addition to the above findings, tryptophan depletion, which causes reductions in brain 5-HT synthesis, has been found to impact on aggression, inattention, behavioural inhibition, impulsivity in children and adolescents diagnosed with ADHD. From a compounding pharmacist perspective, research has strongly indicated that the combination of 5-HT and dopamine amino acid precursors in a recent clinical trial of 85 ADHD patients (aged 4-18 years) resulted in 77 percent of patients showing a significant improvement in the above mentioned symptoms. Since 5-HT and DA amino acid precursors are recognised as safe by the food and drug administration, no safety concerns are associated with this treatment (Hinz, Stein, Weinberg & Unicini, 2012). It is important to note that a script is required for intervention of the above, and must be formally advised by your primary health care provider.
If you have any questions regarding the points outlined this article please feel free to contact:
A: Mark Hinchey Naturopathy, 601 Glebe Road, Adamstown, 2289, New South Wales, Australia
P: 0432234822 or (02) 40235959