SUMMARY Previous work at this hospital and elsewhere has shown that anaemia in toddlers is common and is associated with psychomotor delay. It seemed unclear, however, whether this association was cause and effect or merely due to the same underprivileged environment. A double blind randomised intervention study was, therefore, performed. After an initial assessment 97 children with anaemia (haemoglobin 8-11 g/dl) aged 17-19 months received either iron and vitamin C or vitamin C only (control group) for two months and were then reassessed. The children who received the iron had an increased rate of weight gain and more of them achieved the expected rate of development. While iron deficiency anaemia is unlikely to be the only factor in the slower development of children living in underprivileged circumstances, it can at least be easily identified and treated. Routine child health surveillance in such areas should include a haemoglobin determination.
Parks, Y. A. and Wharton, B. A. (Community Health and Mental Handicap Services, Canterbury; University of Glasgow, Department of Human Nutrition, Glasgow, UK). Iron deficiency and the brain.
There is increasing evidence both from ‘association’ and ‘intervention’ studies that iron deficiency has an adverse effect on brain function In animals and children. The severity and duration of iron deficiency are important in determining the effect on development. Iron replacement therapy has immediate (within 14 days) and long‐term (over 3 months) beneficial effects on behaviour and psychomotor development. The mechanisms for this probably involve a number of biochemical pathways in which iron is essential. These include mitochondrial enzymes and various neurotransmitters. Cytochrome C is reduced by iron deficiency but brain tissue is relatively spared until the deficiency is severe. Levels of neurotransmitters such as noradrenaline, serotonin and dopamine are all altered during iron deficiency and this may explain some of the behavioural and developmental changes that occur.
Sequential measurements of the ventilatory response to a single breath of oxygen delivered during quiet sleep were made in 16 healthy infants between 1 and 3 months of age, alternately breathing air and 16% oxygen in nitrogen. At 1 month the response to a single breath of oxygen during normoxia was a decrease in minute ventilation of 264 +/- 34.2 (SEM) ml.min-1 during the 10-s period following the stimulus (p less than 0.001). During mild hypoxia the decrease in ventilation averaged 471 +/- 49.1 (SEM) ml.min-1 (p less than 0.001). The difference in response between measurements in air and mild hypoxia was significant (p less than 0.001). By the age of 3 months, the absolute ventilatory response to a single breath of oxygen increased significantly in normoxia by 118 +/- 35.2 ml.min-1 (p less than 0.01); the test response to breathing 16% oxygen paralleled the response to normoxia and was on average 254 +/- 26.6 ml.min-1 larger than the response when breathing air (p less than 0.001). When the three age groups were compared, calculating the response per killigram body weight showed that the response was similar at all three ages tested. These data provide a reference baseline for normal infants.
SUMMARY Thirty eight children with a haemoglobin concentration of 106-110 g/l were given either oral iron (n= 17) or placebo (n=21) for two months. The treated group achieved a significantly higher rise in haemoglobin concentration; in a quarter it was greater than 20 g/l. While those with the lower mean corpuscular volume and ferritin showed greater rises in haemoglobin these indices were of little value in predicting response in an individual child.
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