Metabolic effects of a homeopathic formulation of growth hormone (somatomedin-C) in older adults.

It is known that an increase of plasmatic GH 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 peptide hormones like vasopressin, adrenocorticotropic hormone (ACTH), as well as some of its fragments, and melanocyte-stimulating a hormone (x-MSH), stimulate the acute liberation of GH, in such a way that the fraction of the homeopathic foumulation of GH called Hipophisinum could contribute to the effects of liberating GH in this manner. Be that as it may, the effects of these hormones on the liberation of GH are now considered pharmacological effects probably caused by an interaction with the GHRH receptor in the somatotrophs. If this is the case, the homeopathic formulation of GH would exercise its actions at the hepatic level and in the anterior hypophysis.

The administration of GH in hypophysectomized animals and in GH 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 effects observed after only a single injection of GH are bi-phasic: at the beginning there is a decrease in the concentration of glucose in the blood, of free fatty acids and of aminoacids. In a few hours, glucose and aminoacid levels return to normal. The majority of these effects are also observed in humans, although, with more moderate changes. When the acute effects of GH 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 GH forming the basis of diabetogenic effects of GH in the metabolism of carbohydrates and lipids.

The effect the administration of GH 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 effect of GH on beta cells. It can be observed 5 minutes after GH injection both in normal and GH 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 effect and represents a secondary response to the obstacle of utilizing carbohydrates.

In this investigation, Group 1, treated only with 21st Century HGH, 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 GH 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 IGH-I were the significant decrease in the percentage of body fat and weight of the subjects.

continued part 4