I am convinced GHRP 2 , MOD 1-29 and CJC-1295 will help and reverse age related decline in cognition, promote delta wave sleep and increase muscle mass verse fat

GHRH last for 30 minutes or more. This is a fine peptide to contribute to a GH pulse. This I call modified GRF(1-29)

Somatostatin is stopped by GHRPs     very large amounts say 2mg (2000mcg) are sometimes used. Injecting GHRH alone is not very effective

Choose a GHRH to add to the GHRP because it will synergisticly amplify the GH pulse.  How few times can I inject for for some better sleep, small anti-aging effect? Just pre-bed     

Step five: Assess tolerance by dosing just once w/ a GHRP pre-bed at half of saturation dose. Then if that goes well go to full saturation dose. If that goes well add a 2nd dosing, If that is fine add a third dosing.


Step six: Decide on a dose. Saturation dose is defined as either 100mcg or 1mcg/kg of bodyweight in the studies

What are GHRP-6, GHRP-2, Ipamorelin, Hexarelin?


In short they are all forms of GHRPs (Growth Hormone Releasing Peptides, Ghrelin-mimetics

Ghrelin is a hunger derived gut-hormone. It is capable of making its way to the pituitary where the GH releasing cells (somatotrophs) reside. Just like GHRH &Somatostatin it also can contact the cell. When it does it reduces Somatostatins effect. Ghrelin increases GH release. It does this in several ways -by encouraging the brain to release more GHRH, amplifying the effect of GHRH when it gets to the somatotroph, benefiting from GHRH being at the cell to amplify Ghrelin's own effect which is in part an increase in GH release and countering Somatostatin's stoppage effect at the cell.

In fact Ghrelin can cause GH release all by itself even if Somatostatin is around. But Ghrelin makes the environment safe forGHRH to act and if GHRH acts when Ghrelin is there the result is what is called a synergistic GH release

modified GRF(1-29). Since it is basically a 30 minute plus lasting GHRH 

What is CJC-1295, CJC-1293, GRF(1-29), Sermorelin and modified GRF(1-29)?


In short they are all forms of GHRH (Growth Hormone Releasing Hormone).

Datrius B. True use either GHRP-2 or Ipamorelin with modified GRF(1-29) I usually rotate around

Somatotrophs are not cells that release prolactin. Prolactin is released by Lactotrophs

injecting GHRH. There will be zero GH release if somatostatin is around and only some if somatostatin is just starting up 

Wake up! GHRPs are the 3rd hormone/peptide that effects GH release. Its presence at the somatotroph causes GH release on its own and with the naturally occurring "on switch" it amplifies GH release. By stopping somatostatin GH is released. Now GHRPs never result in GH bleed. The release they trigger is always a pulse that is over with within 3 hours.

GHRP-6 is sloppier in that it activates a wider array of effects beyond GH release. It causes intense hunger and gastic motility. It can have a mild effect on cortisol and prolactin. It is a first generation GHRP.


GHRP-2 is less sloppy with a more intense GH release, no gastric motility and less hunger effect. It can have an effect within the normal range on prol

catin and cortisol. 2nd gen


Ipamorelin is not sloppy at all. It does not release as much GH as GHRP-2 but it causes virtually no hunger or gastric motility and for the most part does not effect cortisol or prolactin. 3rd gen


You would choose GHRP-2 unless you wanted GHRP-6 for the hunger effect or for the lower release profiles.


You would choose GHRP-2 normally as the most bang for the buck.    Tom's medical grade peptide   authentiquevie@gmail.com

A simple way to look at it - if you can not keep insulin quiet then that time period really won't be a fatloss time period so don't dose the Mod GRF(1-29)/GHRP for lipolysis (i.e. fatty acid liberation) - if you can not be active during that time to burn off the liberated fat then no need to dose the Mod GRF(1-29)/GHRP because fats will just clutter the blood stream and redeposit.

If insulin will be active and you will have a weight workout then consider using Mod GRF(1-29)/GHRP to effect protein metabolism in an anabolic way and to generate intramuscular growth factors for hypertrophy.

Mod GRF(1-29)/GHRP to effect protein metabolism in an anabolic way and to generate intramuscular growth factors for hypertrophy.

Only carbs and fats blunt GH release so avoid these an hour prior to the shot and 15-20 mins post injection

higher level**********Loose the DAC and you lose the albumin. When this happens the remaining compound some GHRH derivative has more attraction for the receptor, stronger binding and because of the pulsation rather then the elevations less molestation of the receptor and more "oh la la!"

Modified GRF(1-29) also known as "CJC1295 w/o DAC and w/o the extra lysine and then terminated properly

I feel I can tell the difference. If it is a cost issue even 25, 40, 50mcg of GHRH will be synergistic

Only carbs and fats blunt GH release so avoid these an hour prior to the shot and 15-20 mins post injection

 growth hormone ligand binds to a receptor and how these events effect the transcription of proteins inside the cell nucleus. We have discussed growth hormone, IGF-1 and insulin in terms of circulatory levels but we have not examined the extent to which these respective ligand-bound receptors interact with one another to effect protein transcription and in particular tissue growth.

Hormonal pulsation is incredibly important. Pulsation conveys hormonal signals which upon ligand receptor-binding transmits information content to regulators of signaling pathways which go on to effect intracellular happenings.

elderly men and women have equally low amplitude GH pulses and reduced IGF-I levels (24, 38). Based on the known properties of GH and IGF-I in vivo, this reduced amplitude, in combination with reduced sex steroid production, likely explains the observed age-dependent change in metabolism, increased fat/lean ratio, decreased muscle strength, reduced exercise tolerance, and increased bone loss. Hence, the functional deficits that result from aging are probably caused by suboptimal signaling from the hypothalamus. An ideal approach for modifying the aging phenotype would be to restore activity of the hypothalamic neurons that control GH pulse amplitude.

GH increases bone density and improves body composition, cognitive function, cardiac function, and exercise tolerance

 In addition to reduced GH release during aging, the concentration of GH receptors in the brain also declines.

GH-deficient children have an increased incidence of anxiety, depression, and attention deficits, which may contribute to their observed learning disabilities in arithmetic, spelling, and reading compared with age-matched controls (202, 204).GH-deficiency in adults is reported to be associated with reduced energy, unfulfilled personal life, low self-esteem, problems controlling emotional reactions, social isolation, impaired social function, mental fatigue, impaired general and mental health, and deficits in cognitive function (205–211). Markedly reduced GH levels, particularly the integrated nocturnal levels, have also been associated with major depressive illness (212). This may explain the increased incidence of depression and poor sleep quality in the elderly population.

Doses of GH that produced supraphysiological levels of IGF-I normalized memory function after 6 months of treatment. Lower doses selected to provide physiological IGF-I concentrations in the blood improved memory function more slowly, but normal function was restored after 12 months of treatment

IGF-I deficiency could be involved in cognitive deficits seen with aging   When they throw in the term "w/o DAC" they are indicating that they are selling D-Ala2 GRF(1-29) + an unstable lysine

Now if you inject GRF(1-29) into the blood streams enzymes will quickly cleave the peptide at the 2nd position. So GRF(1-29) was altered at the 2nd position to prevent this. That alteration was replacing alanine with its isomer D-alanine. D-Ala2 GRF(1-29) binds to the GHRH receptor as well as GHRH does.

Now to make GRF(1-29) even more resilient 3 more amino acids were changed, bringing the total changes to four (tetra - the Greek cardinal number 4). So a tetra subbed GRF(1-29) known as "Modified GRF(1-29)". Modified GRF(1-29) binds to the GHRH receptor as well as GHRH does.

The outcome was consistent with a protective effect of IGF-I on the onset of age-dependent cognitive deficiencies, particularly in speed of information processing

IGF-I was directly related to information processing speed, memory, fluid intelligence, and Mini Mental State Examination score,

Serum IGF-I appears to regulate brain amyloid-B (AB) levels   

Studies on centenarians showed increased prevalence of dementia in those with lowest serum IGF-I levels

  

However, GH treatment produces increases in IGF-I, reverses the age-dependent changes, and increases the number of cortical arterioles

Indeed, chronic administration of a GHRH analog (D-Ala2-GHRH) prevents age-dependent decline in memory in rats (239)

The CNS effects of GH and GHRH are believed to regulate sleep. Slow Wave Sleep and secretion of GH decrease proportionality during aging 

In addition to having stimulatory effects on GH release, GHRH promotes SWS 

bolus

 iv injection

 and intranasal delivery of GHRH increased REM and SWS in old and young human subjects, whereas slow, continuous infusion was ineffective

The GH/ IGF-I axis plays an important role in regulating metabolism, thymic function, bone density, muscle strength, cardiac function, reproductive function, and CNS function (see SectionV). Although rejuvenation of the GH/IGF-I during aging may not have a profound impact on a single function, subtle improvement in all of these important physiological parameters is likely to have a significant impact on quality of life (see Section V). Reduced amplitude of GH pulsatility during aging causes decreases in serum IGF-I levels and is a result of attenuated GHRH signaling

 Chronic activation of the GHS-R by the small molecule agonist MK- 0677 sustained rejuvenation of the GH/IGF-I axis in elderly subjects (25, 38, 277–280). This is accompanied by increased lean body mass and increased bone mass (38, 281–283). In addition to beneficial effects on peripheral tissues, restoring young adult levels of GH and IGF-I is anticipated to be neuroprotective 

n old rats, l-dopa administration restores the amplitude of GH release to that typical of young rats (36), which is reminiscent of the effects of the GHS-R ligand MK-0677 in elderly humans

Perhaps the most exciting recent observation is that ghrelin activation of the GHS-R on T cells antagonizes production of IL-6 (315). This has extraordinary significance to aging because IL-6 levels increase during aging and in diseases common in the elderly, whereas production of the normal counterregulatory hormones, the sex steroids, GH, and IGF-I, decline 

In addition to having negative effects on CNS function, increases in the IL-6/IGF-I ratio is predictive of mortality in frail, elderly women (3, 316, 329, 330). Hence, treating frail elderly subjects chronically with ghrelin mimetics should improve their quality of life and reduce mortality by lowering IL-6 and increasing IGF-I production.

The earliest manifestations of aging are metabolic changes that result in increased fat deposition and reduced muscle mass, which lead to increased likelihood of developing "metabolic disease" (type II diabetes, hyperlipidemia, arteriosclerosis, and hypertension

Although circulating ghrelin concentrations increase between early adulthood and middle age in humans, there is evidence that old age is associated with decreased ghrelin concentrations in rodents and in humans (311, 346). Therefore, enhanced effects of CCK and/or reduced effects of ghrelin may contribute to the development of anorexia and, in some cases, protein malnutrition during aging.

We discussed previously that chronic treatment of elderly subjects with ghrelin mimetics restores the age-related decline in amplitude of GH pulsatility and circulating IGF-I to levels typical of young adults (25, 38, 279). These results suggest that during aging either ghrelin production declines or ghrelin resistance occurs. The orexigenic property of ghrelin coupled with its anabolic effects via the GH/IGF-I axis and its inhibition of the production of inflammatory cytokines (315) indicate that rescue of reduced GHS-R activity 

The lower ghrelin levels in the old subjects were accompanied by increased insulin levels and low serum IGF-I               In rats, leptin administration selectively decreases visceral fat (VF) by approximately 60% and inhibits hepatic glucose production by approximately 80%

relationship between the age-related increase in Visceral Fat and increased insulin resistance may involve the failure of centrally acting leptin to regulate fat distribution

hese results support the conclusion that aged rats are less responsive to leptin because of impaired suppression of hypothalamic NPY synthesis.

leptin resistance accompanies obesity and in most cases insulin resistance. In nonobese animals, both insulin and leptin act on the hypothalamus to inhibit feeding behavior.

this article was derived from the expertise of Datrius B. True 

http://edrv.endojournals.org/cgi/reprint/26/2/203.pdf       http://www.datbtrue.co.uk/forums/showthread.php?10-Basic-Peptide-Primer

http://edrv.endojournals.org/cgi/reprint/26/2/203.pdf              http://www.datbtrue.co.uk/forums/showthread.php?12-Growth-Hormone-Secretagogues