Children with a height of 2 sd below the mean for age and sex in the general population are defined as having a short stature and are referred to paediatric endocrinology(Reference Deodati and Cianfarani1). In about 20 % of the children with a short stature, a medical explanation for the poor linear growth will be found(Reference Deodati and Cianfarani1, Reference Cohen, Rogol and Deal2). The other 80 % of these children remain without a definitive diagnosis and are labelled as having idiopathic short stature (ISS). ISS is defined as a condition in which the height of an individual is more than 2 sd below the corresponding mean height for a given age, sex and population group, without evidence of systemic, endocrine, nutritional or chromosomal abnormalities(Reference Deodati and Cianfarani1, Reference Cohen, Rogol and Deal2).
Although the process of linear growth is not entirely understood, it is well known that the somatotropic axis play a key role in this(Reference Loveridge and Noble3). The somatotropic axis originates in the hypothalamus region and in the pituitary gland, situated right beneath the hypothalamus. Through the central release of growth hormone (GH), a peripheral production of insulin-like growth factor 1 (IGF-1) is stimulated. IGF-1 receptors are found in proliferating bone chondrocytes, and IGF-1 itself stimulates the synthesis of collagen(Reference Karlberg4). From epidemiological studies it is known that the somatotropic axis is associated with linear growth in infancy, childhood and puberty. Increased IGF-1 concentration and subsequently an increased growth velocity determine the growth curve of each individual child(Reference Juul, Dalgaard and Blum5).
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To increase linear growth in children having ISS, the effect of GH therapy has been studied extensively. A meta-analysis using three randomised controlled trials has shown that the mean adult height was − 1·5 sd score for GH-treated children with ISS and − 2·3 sd score for untreated children with ISS. The adult height achieved by those in the treated group significantly exceeded that of the controls, with a mean difference of 0·65 sd score (about 4 cm)(Reference Deodati and Cianfarani1). The mean duration of therapy was 5·4 (sd 1·5) years(Reference Deodati and Cianfarani1). The cost of height gain attributable to treatment in children with ISS is about $10 000-20 000/cm(Reference Hintz, Attie and Baptista6). At the current time, there is a study demonstrating improved quality of life and better psychological health due to GH/IGF-1 treatment, particularly in children with GH deficiency(Reference Huisman7). However, the benefits of treatment should be balanced with the high cost and unknown side effects of these therapies(Reference Cohen, Rogol and Deal2). Consequently, in several countries, treatment of ISS by GH or IGF-1 treatment is not paid by insurance(Reference Colsman and Sandberg8).
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As an alternative to stimulate linear growth by injections of GH/IGF-1, it is possible to stimulate GH release, and hence growth physiologically. Physiological factors influencing GH release and growth include sleep(Reference Van Cauter, Plat and Copinschi9), exercise(Reference Wideman, Weltman and Hartman10) and diet(Reference van Vught, Nieuwenhuizen and Brummer11, Reference Moller and Jorgensen12). Indeed, from 1982, intravenous arginine administration has been clinically used as a method to assess the responsiveness of the GH secretory system, for example, when GH deficiency is suspected(Reference Biller, Samuels and Zagar13). GH concentration can increase 20-fold after an intravenous arginine bolus (0·5 g/kg)(Reference Biller, Samuels and Zagar13, Reference Merimee, Lillicrap and Rabinowitz14). Additionally, a single oral bolus of arginine has been found to increase GH concentration 2-4·5-fold in adults(Reference Collier, Casey and Kanaley15, Reference Isidori, Lo Monaco and Cappa16).
There is evidence that increased arginine intake increases the GH/IGF-1 release. However, the direct association between habitual dietary arginine intake and linear growth is not well documented. The present study therefore examines the influence of diet, and, in particular, the habitual intake of arginine on growth, while also defining the amount of arginine intake needed for optimal growth in pre-pubertal children. Optimal growth in the present study is defined as the maximum growth velocity.
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