Attention Deficit Hyperactivity Disorder, or ADHD is a common childhood disorder that displays symptoms before the age of 5 and frequently subsides when puberty is reached. As many as 60% ‘grow out of’ ADHD during their secondary school years.
ADHD is so common that over 30% of primary school aged children will have it [1,2]. The disorder affects more boys than girls, with no real explanation why. One statistic showed that boys are four times more likely to have ADHD than girls.
Many of us have heard of ADHD, and even encountered it, but what is the disorder? Why does ADHD manifest itself in its typical symptoms?
ADHD is a disorder that affects the behavioural systems within the brain. It’s believed to be associated with neural development in children. It’s characterized by poor attention and a tendency to be hyperactive. There are three subtypes of the disorder these are:
- Inattentive type.
- Hyperactive-impulsive type.
- Combined inattention and hyperactive impulsive type. 
Symptoms of ADHD
There are two categories of symptoms that refer to the three subtypes of the disorder. These are ‘Inattentiveness’ and ‘Hyperactivity’:
- A need for an ever-changing environment
- Short attention span
- Easily distracted
- Finding long tasks tedious
- Unable to listen to instructions and carry them out as asked.
- Acting without forethought
- Excessive talking and physical movement
- No concept of danger which can lead to impulsive actions
- Inability to concentrate on a task 
The most common form of the disorder is the “Combined inattention and hyperactive impulsive type”, in which the person will have symptoms of both the inattentiveness and hyperactivity category.
What is the cause of ADHD?
ADHD is a polygenic disease, which means it effects more than one gene, therefore the cause of the disorder is difficult to pinpoint.
The Genetic Explanation
ADHD and related disorders such as Tourette’s Syndrome tends to run in the family. This may be because of defective mechanisms in the brain that are hereditary. It has been found that people with ADHD family members are four to five times more likely to develop ADHD symptoms themselves [4,5].
The Poor Parenting Explanation
This is an incredibly offensive and outdated view on what causes ADHD. It was first thought that parents were to blame for ADHD symptoms by not providing enough discipline to the child. This has since been proven to be incorrect. There are no current, well researched and ethically sound studies that suggest parenting has an effect on the development of ADHD .
The Brain Chemistry Explanation
A wealth of research has been conducted in the field of neurochemistry associated with ADHD. It has focused on the ‘old’ and ‘new’ , or ‘neo’ regions of the brain. This include the Caudate Nucleus Frontal Lobe, Basal Ganglia, and the Cerebellum. These areas of the brain are associated with behavioural control.
It has been scientifically proven that imbalance of molecules called neurotransmitters are to blame for such behaviour. The most dominant of which are Dopamine and Serotonin[3,6]. Studies have shown that people with ADHD symptoms have fewer Serotonin and Dopamine receptors. People with ADHD are unable to produce and use these neurotransmitters in the same way as people without ADHD .
Confirmation of the effect that Serotonin in particular has on ADHD is when it is medicated. Selective Serotonin Reuptake Inhibitors (SSRIs) are frequently used, they work by increasing the life of Serotonin the body so it has more time to take effect. Upon administration of SSRIs a vast improvement in symptoms were recorded .
What can be done to improve symptoms?
The “go-to” treatment for ADHD is medication, including methylphenidate (Ritalin) and dexamfetamine, amongst others. All of which focus on the rebalance of neurotransmitters in order to improve attention and behaviour.
More natural ways of treating the disorder is to nourish the body with foods and natural supplements that can induce neurotransmitter production. Dopamine is produced from Phenylalanine, an amino acid. To cause an increase in this it’s best to eat Phenylalnine rich foods such as almonds, avocados and green tea.
Additionally, persuasive work has been done in the field of Serotonin and its effect on ADHD. Serotonin is made via a series of complicated steps starting with Tryptophan, this is then converted to 5-hydroxytryptophan (5-HTP), then to Serotonin. Tryptophan can be consumed in food, such as eggs, cheese, turkey, nuts and seeds. However, one popular and natural supplement is 5-HTP, the middle step for the formation of Serotonin. 5-HTP is extracted from the seeds of the Griffonia Simplicifolia plant which is naturally high in 5-HTP. 5-HTP has been shown to naturally boost Serotonin levels. 5-HTP has been shown to stimulate the faulty serotonin receptors (5HT1-5HT7) to produce and metabolise Serotonin correctly. Additional studies have shown that due to the increase of Serotonin additional symptoms associated with ADHD including sleep disorders and anxiety subside [7,8].
There is no specific dosage listed for ADHD, however a recognised safe dosage for 5-HTP is between 50mg and 200mg dependent on your needs.
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- Brewer, S.Dr. (2002). Attention Deficit Hyperactivity Disorder. London: Constable & Robinson. P.g. 355-357.
- ADDitude. (2016). The Statistics of ADHD. Available: http://www.additudemag.com/adhd-web/article/623.html.
- ADHD Foundation. (2014). What is ADHD. Available: http://www.adhdfoundation.org.uk/whatisadhd.php.
- NHS. (2016). Attention deficit hyperactivity disorder (ADHD) .Available: http://www.nhs.uk/Conditions/Attention-deficit-hyperactivity-disorder/Pages/Introduction.aspx.
- Blum.K, et-al. (2008). Attention-deficit-hyperactivity disorder and reward deficiency syndrome. Journal of Psychiatric Disease and Treatment. 4 (5), Pg. 893-918.
- MyADHD. (2004). Causes of ADHD. Available: http://www.myadhd.com/causesofadhd.html.
- Progressive Health. (2016). 5 HTP and ADHD. Available: http://www.progressivehealth.com/using-5-htp-for-adhd.htm.
- Hinz.M et-al. (2011). Treatment of attention deficit hyperactivity disorder with monoamine amino acid precursors and organic cation transporter assay interpretation. Journal of Neuropsychiatric Disease and Treatment. 7 (2), Pg. 31-38.