Use of dietary supplements and hormones in adolescents: A cautionary tale.

Ergogenic aids, such as nutritional supplements, anabolic steroids and human growth hormone, are increasingly being used to enhance sports performance or body image. While few rigorous scientific studies have derived significant conclusions, the marketing and promotion of most supplements is intense and far exceeds the data supporting their use. Particular concern has arisen regarding safety in the use of these substances among adolescents, who may be at particular risk when using caffeine-ephedra and anabolic steroid combinations. Indeed, long-term effects and fatalities have been reported. As a consequence, the American Academy of Pediatrics has condemned the use of anabolic steroid use for bodybuilding or performance enhancement in adolescents. Health care professionals need to educate themselves about ergogenic use and ask informed questions of their adolescent patients. An honest discussion of the limitations of most supplements, and acknowledgement that some supplements may work some of the time, may allow the physician to be more credible and useful in providing medical care and guidance to the adolescent seeking to improve body image or athletic performance.

Indicators of adult height outcome in classical 21-hydroxylase deficiency congenital adrenal hyperplasia.

OBJECTIVE: To obtain objective information on the relationship between adult height (AH), glucocorticoid (GC) dose, and degree of hormonal suppression in a population of patients with 21-hydroxylase deficiency congenital adrenal hyperplasia (21-OHD CAH) to optimize treatment regimes. STUDY DESIGN: Multicenter retrospective chart review of patients with salt wasting 21-OHD CAH diagnosed in the first 6 months of life, and who had reached AH (n = 54). The data were compiled into a single database. RESULTS: Mean adult height standard deviation score - midparental height standard deviation score was -1.1 for both sexes. Growth velocity was normal during childhood but compromised during infancy and puberty. Onset and tempo of puberty were normal-to-delayed. Bone age was closely correlated with chronologic age (r = 0.93). AH was negatively correlated with androstenedione in infancy (r -0.68; P =.03) and childhood (-0.66; P <.01) and with testosterone in childhood (r -0.44; P =.01), but not with dehydroepiandrosterone or 17-hydroxyprogesterone. GC dose was not associated with AH. CONCLUSIONS: Mean AH was in the lower range of genetic potential in this group of persons with 21-OHD CAH. Androgen levels should be used in conjunction with growth velocity measurements to optimize GC dosing in persons with 21-OHD CAH.