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Parenteral administration of human chorionic gonadotropin (hCG) or luteinizing hormone (LH) stimulates the production of testosterone in males and these gonadotropins can therefore be used by athletes to enhance muscle strength. However, they are more expensive and less efficient than testosterone and anabolic steroids. Therefore their main use is probably to stimulate gonadal testosterone production during and after self-administration of testosterone or anabolic steroids. A positive effect of hCG on muscle strength has not been demonstrated in women and elevated concentrations of hCG in females are often caused by pregnancy. The use of gonadotropins is therefore prohibited only in males but not in females. HCG occurs at low but measurable concentrations in plasma and urine of healthy males and can be measured by sensitive methods. However, the characteristics of the method to be used for doping control have not been defined. Virtually all commercially available hCG assays have been designed for determination of hCG in serum rather than urine, which is used for doping control. Methods based on mass spectrometric detection of fragments derived from hCG extracted from urine by immunoadsorption have been developed but their suitability for doping control remains to be determined. The concentrations of LH in serum and urine are variable and more then 10-fold higher than those hCG. It is therefore difficult to detect illicit use of LH. The characteristics and reference values for hCG and LH assays used in doping control and the cutoff values need to be defined. (2008) Keywords: gonadotropins; hCG; LH; immunoassay; mass spectrometry; doping control; doping Abbreviations: CTP, C-terminal peptide; ESI, electro spray ionization; FSH, follicle stimulating hormone; hCG, human chorionic gonadotropin; hCGn, nicked human chorionic gonadotropin; hCGb, free b subunit of hCG; hCGbn, nicked free b subunit of hCG; hCGa, free a subunit of hCG; hCGh, hyperglycosylated hCG; hCGbcf, core fragment of hCGb; GnRH, gonadotropin releasing hormone; GPH, glycoprotein hormone; GPHa, free a subunit of glycoprotein hormones; hCGa, free a subunit of hCG; IU, international unit; LH, luteinizing hormone; MALDI-TOF, matrix-assisted laser desorption and ionization-time of flight; MS, Mass spectrometry; rhLH, recombinant human LH; rhCG, recombinant human chorionic gonadotropin; TSH, thyroid-stimulating hormone British Journal of Pharmacology

The short-term effects of rye bran bread intake in prostate cancer were investigated. Ten men with conservatively treated prostate cancer were randomised to a daily supplement of 295 g of rye bran bread and eight men to 275 g of wheat bread (control) with similar fibre content for three weeks. Blood samples, ultrasound-guided core biopsies of the prostate, and urine samples were taken. In the rye group, there was a significant increase in plasma enterolactone, and the apoptotic index increased significantly from 2.1% (SD 1.3) to 5.9% (SD 1.8), P<0.005 as measured by a TUNEL index in four cases in the rye group and seven cases in the control group. Besides a significant decrease in weight in both groups, only small changes were observed in plasma concentrations of prostate specific antigen (PSA), circulating sex hormones, excreted oestrogens, insulin-like growth factor (IGF)-I, and in the endothelial fibrinolytical system. High intake of rye bran bread is suggested to increase apoptosis in prostate tumours.

Our aim was to assess adrenocortical function in very low birth weight infants, specifically to evaluate the impact of gestational age and dexamethasone (DEX) therapy on serum concentrations of total and free cortisol, dehydroepiandrosterone sulfate (DHEAS), and steroid-binding globulins. Twelve moderately preterm or full-term neonates of 38 +/- 4 (mean +/- SD) wk of gestation and 36 ill preterm neonates of 26 +/- 2 (mean +/- SD) wk of gestation were studied. Twenty-three of the 36 ill preterm neonates participated in a randomized neonatal DEX trial for the treatment of early chronic lung disease and received a 1-wk treatment of DEX or placebo. Serum concentrations of cortisol, corticosteroid-binding globulin (CBG), sex hormone-binding globulin (SHBG), and DHEAS were measured, and an ACTH test was performed. Gestational age correlated with the umbilical cord concentrations of total cortisol (r = 0.702, p < 0.01), free cortisol (r = 0.489, p < 0.05), DHEAS (r = 0.608, p < 0.01), and SHBG (r = 0.831, p < 0.01), but not significantly with the concentration of CBG (r = 0.428, p = 0.076). One-week DEX therapy decreased the serum concentrations of CBG (DEX 295 nmol/L, placebo 504 nmol/L; p < 0.01), DHEAS (DEX 6.5 mumol/L, placebo 11.8 mumol/L; p < 0.05), and the basal (DEX 81 nmol/L, placebo 176 nmol/L; p < 0.01) and ACTH-stimulated cortisol levels (DEX 458 nmol/L, placebo 817 nmol/L; p < 0.05). One week after discontinuation of DEX or placebo, basal cortisol concentrations did not differ significantly, but ACTH-stimulated cortisol levels were lower in the DEX-treated than in the placebo-treated infants. DEX therapy decreased the serum CBG and DHEAS concentrations and caused a transient suppression in the adrenocortical function. Despite severe illness, the very preterm neonates had relatively low basal cortisol concentrations, suggesting their reduced ability to respond adequately to stress during intensive care.