It is known that an increase of plasmatic HGH acts as a negative feedback mechanism inhibiting the liberation of GH by the hypophysis,3s stimulating the secretion of somatostatin (SRIF) and inhibiting that of GHRH. Nevertheless, it is also known that various peptides like vasopressin, adrenocorticotropic hormone (ACTH), as well as some of its fragments, and melanocyte-stimulating a hormone (x-MSH), stimulate the acute liberation of human growth hormone, in such a way that the fraction of the homeopathic formulation called Hipophisinum could contribute to liberating HGH in this manner. Be that as it may, the effects on the liberation are now considered pharmacological responses probably caused by an interaction with the GHRH receptor in the somatotrophs. If this is the case, the homeopathic formulation would exercise its actions at the hepatic level and in the anterior hypophysis.
The administration of HGH in hypophysectomized animals and in human growth hormone deficient humans is followed in a few days by a positive balance of nitrogen, a decrease in the production of urea, and in the quantity of body fat, as well as in a reduction of glucose utilization. The results observed after only a single injection of HGH are bi-phasic: at the beginning there is a decrease in the concentration of glucose in the blood, of free fatty acids and of amino acids. In a few hours, glucose and amino acid levels return to normal. The majority of these results are also observed in humans, although, with more moderate changes. When the acute results disappear, a series of delayed effects appear which include: a) an increase in the mobilization of free fatty acids from adipose tissue, as a consequence of the lipolysis of triglycerides; b) an increase in the sensitivity to lipolytic effects of catecholamines; and c) inhibition not only in castration but also in the utilization of glucose. These effects last for many hours and accumulate with additional exposures to human growth hormone forming the basis of diabetogenic effects of HGH in the metabolism of carbohydrates and lipids.
The result the administration of HGH has on the secretion of insulin is complex and seems to be tri-phasic. Initially, there is an increase in the release of insulin, which seems to be a direct result of human growth hormone on beta cells. It can be observed 5 minutes after HGH injection both in normal and deficient subjects. In the following 1 to 5 hours, there is slight inhibition in the secretion of insulin. Greater and more persistent increases of glucose can be seen in prolonged treatments; this is an indirect result and represents a secondary response to the obstacle of utilizing carbohydrates.
In this investigation, Group 1, treated only with 21st Century human growth hormone, showed a statistically significant increase of glucose which was not seen in Group 2, treated with a combination of 21st Century HGH plus HE. Be that as it may, this process is reversible once suspended or when HGH influence decreases. The secretory capacity of beta cells does not seem to be erroneously compromised.
Other changes that we observed as a consequence on the increase in IGF-1 were the significant decrease in the percentage of body fat and weight of the subjects.
Continued Part 4: Human Growth Hormone Aging