A lot of myths surround injectable hGH and its effects on athletes. Here are some risks you should be aware of. If you buy what may be called "growth hormone," "growth stimulator" or "growth factors" online, it's likely they're not really hGH. Many websites claim to be selling growth hormone, but they're really selling amino acids that don't significantly increase growth hormone levels in your body. Also there's a risk of contracting HIV or other diseases (like hepatitis) if people share needles, because human growth hormone can only be injected, like many steroids.
When the diagnosis of IUGR has been established, it is helpful to determine a specific etiology. Therapy may be nonspecific but should try to address the underlying cause. Many infants thought to be growth-retarded are, in retrospect, found to be constitutionally small. The key management issues are the gestational age of the pregnancy at the time of diagnosis and the urgency to expedite delivery. Most fetal deaths involving IUGR occur after 36 weeks of gestation and before labor begins. 1 The clinician must balance the risk of delivering a premature infant against the potential for intrauterine demise.
Exposure of the normally grown fetus to antenatal glucocorticoids can cause a decrease in brain growth and maturation [ 65 , 68 , 97 , 98 ], but not in nutrient transport [ 99 , 100 ] or protein synthesis [ 66 ]. In sheep, both exogenous and endogenous glucocorticoids decrease blood brain barrier permeability in the sheep fetus at 60% but not 90% of gestation [ 101 ]. In addition to its role in the placenta, P-gp is an important component in protecting the fetal brain from exposure to drugs [ 102 ]. Brain sparing, defined as an increased brain to body weight ratio, is a notable characteristic of IUGR babies; yet little is known about the impact of IUGR on the expression of drug transporters on the blood brain barrier. In contrast to the effects in the placenta, dexamethasone increases P-gp mRNA and protein expression in rat brain endothelial cells in vitro [ 91 , 103 ]. Similarly, BCRP mRNA and protein expression in rat brain endothelial cells increases in response to dexamethasone in vitro [ 103 ]. However, it is not known whether there will be similar changes in P-gp expression in the brain of IUGR fetuses because they already have elevated plasma cortisol concentrations [ 44 , 104 ]. If P-gp expression in the blood brain barrier is altered by IUGR, this has implications for the potential toxicity of drugs used in the management of preterm delivery, maternal hypertension, gestational diabetes, and viral infections. For example, we have shown that IUGR as a result of maternal undernutrition before conception and throughout pregnancy in the guinea pig results in decreased P-gp protein [ 92 ] and BCRP; mRNA expression in the brain (Figures 1(b) and 2(b) ). Hence, administering dexamethasone or betamethasone to the preterm IUGR fetus may further decrease the protective effects of P-gp and BCRP, although, further studies are required to verify this.