Theoretical considerations suggest that iron deficiency (ID) may play a role in the pathophysiology of ADHD, at least in a subgroup of patients. The ID hypothesis is grounded on several lines of evidence.
(i) Iron is a coenzyme necessary for synthesis and catabolism of monoaminergic
neurotransmitters that are implicated in ADHD pathophysiology.
(ii) ID is associated with decreased dopamine transporter expression. Variation in the
corresponding dopamine transporter gene has been linked to genetic vulnerability for
(iii) ID may lead to dysfunction in the basal ganglia, which has been implicated in the
pathophysiology of ADHD.
(iv) ID has been reported in children with cognitive and behavioural impairments that
include poor attention and hyperactivity.
Peripheral (i.e. in the body) iron status may be estimated by serum ferritin levels. To date, several studies assessing serum ferritin levels in children with ADHD have been published with controversial results. For example, of 11 published studies, seven have found an inverse significant relationship between serum ferritin and ADHD symptom severity, whereas four additional studies failed to confirm this significant relationship. One possible explanation that may reconcile these apparently contradictory findings focuses on the role of brain iron deficiency. Since it is brain iron that impacts neurotransmitter levels, researchers have suggested that it is low brain iron, not necessarily peripheral iron, that increases the risk of developing ADHD. However, it is also possible that a dysfunction in the blood brain barrier, which regulates the entry of iron into the brain, can also lead to low brain iron levels despite peripheral iron remaining normal.
Reinforcing this view is evidence from the study of another disorder, namely, restless leg syndrome (RLS). It is well known that ADHD may be comorbid with sleep disorders including RLS. It has been noted in recent times that the activity of the iron regulatory protein 1, which regulates the entry of iron across the blood brain barrier is decreased in the brain microvasculature of individuals diagnosed with RLS. It has been proposed that the endothelial cells of the blood brain barrier represent an iron reservoir for the brain and that the underlying problems in RLS is the lack of sufficient reserve to meet physiological challenges, such as circadian changes in serum iron. Given this deficit in iron transport and storage within the brain microvasculature endothelial cells, brain iron levels in RLS may be inappropriate for brain functioning even in the presence of normal peripheral iron levels. Moreover, low peripheral iron status may further decrease brain iron levels for individuals diagnosed with RLS. It is by way of this comparable hypotheses that low brain iron may increase risk for ADHD.
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