Secretagogues are the  p recursors of Human Growth Hormone. Higher HGH levels  will increase muscle, reduce wrinkles improve cardiac output, enhance memory levels, tighten the skin, decrease body fat and increase lean body mass. These new  secretagogue proucts are amazing...I have been on them several months now and am rejeuvenated...a new younger person, Anyone else here have experience with  secretagogues? Would like to compare notes..POST _script_...Secretagogues work by stimulating the petuitary gland into producing HGH.

Higher HGH levels  will increase muscle, reduce wrinkles improve cardiac output, enhance memory levels, tighten the skin, decrease body fat and increase lean body mass. Higher GH may also stimulate dormant or pre-cancerous cells to grow and divide. Also no one knows if any of these beneficial changes will remain for very long nor whether life will be extended or shortened by the use of GH. I suggest being very cautious concerning GH increase.

Secretagogues are the  p recursors of Human Growth Hormone. No. The reason for reduced serum GH with age is not its production. And in any case it is a complex protein which has multiple amino acids as precursors . The reason for its reduced serum levels with age is that its secretion from the pitutitary where it is made is decreased. Hence, the name for certain chemicals which may increase this secretion of a hormone which is ready and waiting in the pituitary but can't get out. Tom, Do you know how this was determined?  It seems to me that if production is the same, but secretion is reduced, then GH will accumulate in the pituitary until production is shut down, or the gland will swell with stored GH.  I assume it doesn't go so far as to make the gland grow to ridiculous sizes....is the idea that secretion is reduced _base_d simply on a high content of GH in the pituitary of old people? Alex

Secretagogues are the  p recursors of Human Growth Hormone. No. The reason for reduced serum GH with age is not its production. And in any case it is a complex protein which has multiple amino acids as precursors . The reason for its reduced serum levels with age is that its secretion from the pitutitary where it is made is decreased. Hence, the name for certain chemicals which may increase this secretion of a hormone which is ready and waiting in the pituitary but can't get out. Tom, Sorry to be so long getting back to you.   Do you know how this was determined?   It seems to me that if production is   the same, but secretion is reduced, then GH will accumulate in the   pituitary until production is shut down, or the gland will swell with   stored GH. I think the former is true. I don't think the gland does any great amount of swelling.   I assume it doesn't go so far as to make the gland grow to   ridiculous sizes....is the idea that secretion is reduced _base_d   simply on a high content of GH in the pituitary of old people? Perhaps what I said needs to be restated a bit. As explained secretagogues are certainly not precursors in the sense that GH is synthesized from them. This holds not only for simple amino acids such as arginine which is well proven to induce GH secretion when given IV, but also for complex molecules like the natural releaser GHRH (growth hormone secreting hormone). Instead, these are promoters of the production and release of GH. It is my understanding from much reading that the ability to produce GH does not decline in old age, but only the ability to secrete it. This is why aged humans have no problem producing (and secreting) it when they are given effective secretagogues (such as GHRH). Thus, the reduction of GH in old age appears to be mainly caused by a reduction of GHRH, and possibly an increase of GHIH (growth hormone inhibitory hormone - also called somatostatin), both of which are produced by the hypothalmus. I had trouble finding papers to substantiate the above directly. Here is one which may do so in its full text. It also shows that even under equal stimulation by GHRH, many parameters related to GH pharmacokinetics do change with age. Life Sci  1990;47(21):1887-93 Pharmacokinetics of growth hormone secretion in humans induced by growth hormone releasing hormone. Gupta SK, Krishnan RR, Ellinwood EH, Ritchie JC, Nemeroff CB. Department of Psychiatry, Duke University Medical Center, Durham, NC 27710. This investigation compares the age- and sex-related changes in growth hormone (GH) response to growth hormone releasing hormone (GHRH) in normal subjects using an appropriate pharmacokinetic model. Twenty-five subjects (14 males and 11 females) aged 23-89 yr received a single intravenous bolus dose (1 microgram/kg) of GHRH-40 solution. Plasma GH concentration-time profiles are best characterized by a biexponential equation (or one-compartment model) with first-order release and disappearance rates and an equilibration lag time. The harmonic mean release rate half-life is similar for both sexes (males: 12.6 min vs. females; 11.4 min) but significantly different across age groups (23-35 yr: 7.2 min vs. 50-89 yr: 16.8 min). The mean disappearance rate half-life and GHRH-equilibration time lag for females (33.6 and 20.4 min, respectively) and the higher age group subjects (32.4 and 21.6 min, respectively) are significantly longer than those of males (22.8 and 9 min, respectively) and the lower age-group subjects (21.6 and 8.4 min, respectively). The mean _meta_bolic clearance rate of GH is significantly lower (p less than 0.02) for females than for males (3.1 vs. 4.83 ml/hr.m2). However, the production rate and the amount of GH released by the pituitary for our subjects appear to be very similar for both males (8.7 micrograms/hr.m2 and 4.65 micrograms/m2) and females (9.33 micrograms/hr.m2 and 5.11 micrograms/m2). PMID: 2266772 The following paper found that GH production is not negatively correlated with age (but was with adiposity) when stimulated by pyridostigmine, even though, as above, other GH related parameters do change with age. Eur J Endocrinol  1997 Oct;137(4):377-86 Comment in:   Eur J Endocrinol. 1997 Oct;137(4):338-42. Pyridostigmine treatment selectively amplifies the mass of GH secreted per burst without altering GH burst frequency, half-life, basal GH secretion or the orderliness of GH release. Friend K, Iranmanesh A, Login IS, Veldhuis JD. Endocrine Section, Veterans Affairs Medical Center, Salem, Virginia 24153, USA. Growth hormone (GH) release from the anterior pituitary gland is predominantly regulated by the two antagonistic hypothalamic peptides, growth hormone-releasing hormone (GHRH) and somatostatin. Appraising endogenous GHRH action is thus made difficult by the confounding effects of (variable) hypothalamic somatostatin inhibitory tone. Accordingly, to evaluate endogenous GHRH actions, we used a clinical model of presumptively acute endogenous somatostatin withdrawal with concomitant GHRH release. To this end, we administered in randomized order placebo or the indirect cholinergic agonist, pyridostigmine, for 48 h to 13 healthy men of varying ages (29-77 years) and body mass indices (21-47 kg/m2). We sampled blood at 10-min intervals for 48 h during both placebo and pyridostigmine (60 mg orally every 6 h) administration, and used an ultrasensitive GH chemiluminescence assay (sensitivity 0.0002-0.005 microgram/l) to capture GH pulse profiles. Multiparameter deconvolution analysis was applied to quantitate the number, amplitude, mass, and duration of significant underlying GH secretory bursts, and simultaneously estimate the GH half-life and concurrent basal GH secretion. Approximate entropy was utilized as a novel regularity statistic to quantify the relative orderliness of the hormone release process. All measures of GH secretion/half-life and orderliness were statistically invariant across the two consecutive 24-h placebo sessions. In contrast, pyridostigmine treatment significantly increased the mean serum GH concentration from 0.23 +/- 0.054 microgram/l during placebo to 0.45 +/- 0.072 microgram/l during the first day of treatment (P < 0.01). There was also a significant rise in the calculated 24-h pulsatile GH production rate from 8.9 +/- 1.7 micrograms/l/day on placebo to 27 +/- 5.6 micrograms/l/day during active drug treatment (P < 0.01). Pyridostigmine significantly and selectively amplified GH secretory burst mass to 1.5 +/- 0.35 micrograms/l compared with 0.74 +/- 0.19 microgram/l on placebo (P < 0.01). This was attributable to stimulation of GH secretory burst amplitude (maximal rate of GH secretion attained within the release episode) with no prolongation of estimated burst duration. Basal GH secretion and approximate entropy were not altered by pyridostigmine. However, age was strongly related to more disorderly GH release during both days of pyridostigmine treatment (r = +0.79, P = 0.0013). During the second 24-h of continued pyridostigmine treatment, most GH secretory parameters decreased by 15-50%, but in several instances remained significantly elevated above placebo. Body mass index, but not age, was a significantly negative correlate of the pyridostigmine-stimulated increase in GH secretion (r = -0.65, P = 0.017). In summary, assuming that somatostatin is withdrawn and (rebound) GHRH release is stimulated via pyridostigmine administration, we infer that relatively unopposed GHRH action principally controls GH secretory burst mass and amplitude, rather than apparent GH secretory pulse duration, the basal GH secretion rate, or the serial regularity/orderliness of the GH release process in the human. Moreover, we infer that increasing age is accompanied by greater disorderliness of somatostatin-withdrawn GHRH, and hence rebound GH, release. The strongly negative correlation between pyridostigmine-stimulated GH secretion and body mass index (but not age) further indicates that increased relative adiposity may result in decreased effective (somatostatin-withdrawn) endogenous GHRH stimulus strength. Publication Types: Clinical Trial Randomized Controlled Trial PMID: 9368506 This is quite different that a decrease of a chemical being caused by a decrease in one of its precursors from which it is synthesized, or being able to be increased by an increase in such a precursor. It is also different than a decrease of insulin or a sex hormone due to a loss of production capability for some reason such as age.