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In the present state of knowledge,
all that we have been able to do is to trace events back from a rather severe state of
malnutrition. This is not really relevant to the important question: what is the effect of
more moderate degrees of energy deficiency on the metabolic rate and voluntary physical
activity of children? One way of answering this question would be by a cross-sectional
study using doubly-labelled water. An alternative, which would have some advantages, would
be a prospective longitudinal study in a group of children, some members of which could be
expected to be undernourished, and in which measurements of MR and spontaneous physical
activity were repeated at intervals. I believe that such a study would be feasible in a
suitably chosen population and that it would be ethically justifiable provided that the
children were kept under careful observation, that there were facilities for medical care,
and that no child's weight was allowed to fall below 80% of reference weight-for-height.
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The thesis that physical activity is the first outcome to be compromised, while body mass and composition remain protected, was questioned. Does the child really have the ability to perceive a decrease in energy intake and to reduce physical activity before it draws on its fat stores? Waterlow responded that he was basing his hypothesis on the Rutishauser & Whitehead and Torun studies, where physical activity was reduced while growth remained normal.
The potential significance of decreased ion pumping in potassium-deficient children was raised. Is there a correlation with metabolic rate? In this respect, why was adaptation to a hypocaloric diet not listed in the hierarchy of responses to undernutrition? Waterlow responded that there was little data in children and that extrapolation from the Keys-type deprivation studies in adults may not be justified.
Scrimshaw pointed out that there was often a confusion between stunting as being short for one's age and stunting as a below average growth rate. INCAP children over 2 years of age were found to grow normally. One of the early mistakes had been to bring children with low weight-for-age but normal weight-for-height into rehabilitation centres where they gained extra weight, but not height, and therefore became obese.
The difficulty of working with a hypothetical situation of simple energy restriction was highlighted. We may need to consider specific substrates. Reduction in the flow of certain substrates may affect the brain and cause a reduction in activity; others may not, even in isocaloric circumstances.
Jackson returned to the Torun data on children fed different levels of energy and proposed an explanation for the positive nitrogen balance at 70 kcal/kg and evidence for adaptation to a hypocaloric diet. The order of the dietary periods was 100 followed by 70 followed by 80 kcal/d. Children gained weight on 100 kcal/d. At 70 kcal/d they stopped growing and re-established positive nitrogen balance by the end of the 7-day period. When the intake was then raised to 80 kcal/kg the infants gained weight at the same rate as when they were on 100 kcal/kg. The only logical interpretation seemed to be that some form of accommodation to the 70 kcal/kg had occurred, and that this was carried through to the subsequent period. In these studies, stool frequency was 1.5, 0.5 and 0.5 stools per day in the three dietary periods. Taken together with the data presented earlier on urea salvage, this suggested that the gastro-intestinal tract may have a major role in metabolic exchange, the disturbance of which may have many of the effects described in the paper by Scrimshaw.
Caution was urged in looking for associations between energy restriction, activity levels and learning. Acute changes in energy intake may cause distress and depression which may be passed on to the children and may actually cause differences in the biochemical response of the child.
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