Using tritiated glycine (glycine 3H) as an indicator of amino acid incorporation in protein synthesis in cartilage matrices, Mankin and Conger injected hydrocortisone acetate into rabbit knees. Their data showed a rapid and profound decrease in glycine incorporation that appeared to depend on dosages. Maximum decline was seen six hours after the injection. 28 They did a similar experiment using glycine 14C as the radiotracer, which showed a definite decrease in the rate of protein synthesis within two hours of the injection. They noted that the rate of the inhibitory effect of intraarticular hydrocortisone on cartilage protein synthesis was about twice that of the observed rate for corticosteroids given by intramuscular route. 29 One year later, researchers injected hydrocortisone into normal rabbit knees and produced thinning of the cartilage, and the development of fissures and fibrillations in the articular cartilage. They also found multiple small white deposits within the substance of the articular cartilage, which were found to represent cystic areas of degeneration within the middle zone of the cartilage matrix. These effects were most marked in the animals which had the greatest number of injections. 30 Deleterious effects of cortisone were reported by some researchers who noted that the drug inhibited the synthesis and deposition of chondroitin sulfate in cartilage. 31-33
What's more, activating the aggression system turns on the adrenocortical stress response without actual fighting--or even someone to fight. A hypothetical picture emerges: First, as has long been known, a signal from the nervous system (via pituitary hormone ACTH) signals the adrenals to produce a corticosteroid response that prepares the body for an emergency response, popularly called "fight or flight." Second, in this new finding, the same corticosteroid signal also feeds back to the brain, which lowers attack thresholds and facilitates fighting. Fighting, itself a stressor, then further activates the stress response. And so it goes.
There are no available data on the presence of fluticasone propionate in human milk, the effects on the breastfed child, or the effects on milk production. Other corticosteroids have been detected in human milk. However, fluticasone propionate concentrations in plasma after inhaled therapeutic doses are low and therefore concentrations in human breast milk are likely to be correspondingly low [see Clinical Pharmacology ()] . The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for Flovent HFA and any potential adverse effects on the breastfed child from Flovent HFA or from the underlying maternal condition.