Iron is an essential trace mineral in man. The most well known role for iron in humans is its presence in the haemoglobin molecule where it facilitates the transport of oxygen from the lungs to the tissues, and in myoglobin in skeletal muscle where it facilitates the uptake of oxygen for energy production. However, iron has a number of other roles in human metabolism including the metabolism of catecholamines. In this role, iron is required as a cofactor in the tyrosine hydroxylase enzyme, which is the rate limiting step in the synthesis of adrenaline, dopamine and noradrenaline from phenylalanine. Evidence suggests that iron deficiency is associated with changes to catecholamine synthesis, and it has been postulated that at least some of the symptoms of iron deficiency are related to these changes in catecholamine metabolism. Because catecholamines are required for arousal, motivation and energy production, the lethargy associated with iron deficiency may result from decreased central nervous system catecholamine synthesis.
Because of the requirement for iron in the tyrosine hydroxylase enzyme, researchers have investigated the effect of iron deficiency and stress on catecholamine formation. Much of this work has relied on rats but human studies have also been performed. For example, in one animals study1, rats were randomly assigned to receive a diet containing either 6 or 50 mg per kg body weight iron. After three to five days, anaemia developed in some of the rats and the urinary noradrenaline concentrations became elevated in the iron deficient rats compared to control rats. After ten days, the iron deficient rats experiences a fall in urinary dopamine compared to the control rats. When the authors subjected the rats to surgical stress at 38 days of age, noradrenaline and dopamine levels rose suggesting that an acute stress response had been activated. However, the noradrenaline remained significantly higher and the dopamine significantly lower in the iron deficient rats compared to the control rats.
These results support the viewpoint that iron deficiency is associated with changes to normal catecholamine metabolism. Similar results have been reported to occur in man, suggesting that the rat model may be close to that of the human model. Because catecholamines are required for the acute response to stress, the changes in catecholamine metabolism seen in iron deficiency may decrease the ability to cope with stress. It is known that poor iron status is associated with obesity, and this suggests that one of the symptoms of obesity may be changes to catecholamine metabolism. The obese have a blunted thermic effect of food, which is characterised by decreased circulating catecholamine levels (here). Therefore the poor iron status seen in cases of obesity may be linked to the inability to efficiently oxidise excess food postprandially. Changes to catecholamine metabolism therefore explains at least in part some of the symptoms of obesity and may explain behavioural changes seen in cases of iron-deficient anaemia.
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