Also without adequate hGH your tendons and ligaments don’t heal like they do in our youth. When combined with BPC 157 which is purported to be a hGH receptor agonist in tendons and ligaments, hGH can then be more effective in healing those tissues. IF you have any being produced at ones age, mine would be near zero at 69y/o.
As someone who suffered for years with nagging tendon issues, which have resolved over the past 18 months, I’m super happy to be basically pain free and with full range of motion restored.
Even the crunching in my neck that was there for 6 or 7 years is gone.
Quality of life is my goal. Not “longevity”
To be clear, I personally would not use Somatotropin. I’m more interested in having my systems do their job and produce hGH “naturally” at the right time in the circadian/hormonal cycle.
4 Likes
LukeMV
#62
I still say all that improved quality of life will lead to better longevity in the end
4 Likes
Neo
#64
Sounds good - it’s just to me that this does not feel like one of those 50/50 cases
For anyone new to the topic - and to both @Steve_Combi and @LukeMV
See below how for geroscientists, human data, investors and at least for dog, the FDA suggest that lower IGF-1 or IGF-1 inhibition is pro longevity.
If your goals are short term health, muscle building, perhaps wound healing the answer might be difference. For longevity the data seems to line up more in one way than the other
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Neo
#65
Again if you talk with Greg Fahy the developer of this protocol (I have many times), he will be the first to tell you:
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the befits are from the Thymus regeneration itself and the immune benefits
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having to use GH is in order to get that generation, not because they wanted for other reasons to increase people’s GH (perhaps even despite)
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given that they designed it so the growth hormone is only given during a very limited period of time, and with hope of not having to repeat more than a few times during one’s entire life
so for the VAST majority of the time, their patients DO NOT supplement with GH
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And neither do I…
From the paper I provided above
GHRH and GHS stimulate the secretion of GH. Since most AGHD is caused by pituitary lesions, and these patients, unlike healthy seniors, are unresponsive to GHRH or GHS, there are few studies of treatment with these agents.
Theoretically, treatment with GHRH or GHS should lead to more physiologic GH replacement, leading to a pulsatile rather than prolonged elevation in GH and preserving the ability for negative feedback inhibition of GH by increasing IGF-I. GHRH and GHS effects are influenced by the same factors which modulate endogenous GHRH secretion, such as negative feedback by somatostatin. This normal negative feedback regulation would be expected to result in buffering against overdose. The side effects of GHRH treatment are similar in character to GH treatment but are milder and less frequent. Since the GHS are smaller molecules than GH, and generally resistant to digestive enzymes, they can be administered via the oral, transdermal or nasal routes.
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From the paper I referenced.
Mechanistic insights into the role of growth hormone and IGF-I in age-related alterations in cognitive function were assessed in several studies by Sonntag and colleagues demonstrating somatotrophic effects on rodent brain aging (26). These studies suggest that deficiencies in GH and IGF-I contribute to the functional decline in senescent rats whereas augmentation of GH or IGF-I improved cognitive function, increased glucose utilization throughout the brain, increased cortical vascularity, and ameliorated age-related decline in hippocampal neurogenesis**.**
A 2006 study of the effects of 6-months daily treatment with sermorelin acetate, a GHRH analogue, on cognitive function of 89 elderly adults found significant improvement on several cognitive assessments, particularly those involving problem solving, psychomotor processing speed, and working memory, but no change on tests reflecting crystallized intelligence (27). Higher GH levels were associated with higher Wechsler Adult Intelligence Scale performance IQ scores, and greater increases in IGF-1 were associated with higher verbal fluency test scores, while gender, estrogen status, and initial cognitive function did not interact with the GHRH effect on cognition.
A 2013 pilot study of 30 elderly adults given a stabilized analogue of GHRH, tesamorelin, versus placebo, used magnetic resonance spectroscopy to examine the effects of inhibitory and excitatory neurotransmitters (60). After 20 weeks GABA levels were increased in all brain regions, N-acetylaspartylglutamate levels were increased in the dorsolateral frontal cortex, and myo-inositol (an osmolyte linked to Alzheimer disease) levels were decreased in the posterior cingulate, with similar results across adults with mild cognitive impairment (MCI) and those with normal cognitive function. Treatment related changes in serum IGF-1 were positively correlated with changes in GABA and negatively correlated with myo-inositol. There was a favorable treatment effect on cognition (p = .03), but no significant associations were observed between treatment-related changes in neurochemical and cognitive outcomes.
1 Like
mccoy
#68
BPC-157: Is that just a local effect on some specific tissue or a systemic effect as well? I am one of those who suffer from nagging tendons issues when lifting weights, and I hate it.
What is the usual dosage to target the issue of aches in connective tissues?
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That is purported to be systemic, and people suggest to inject near the site of injury if possible. The dosage is usually quite low, and so is the half life (2 hours ). There are a variety of dosages.
For acute injuries, they recommend 200-500 mcg twice a day for a week or two. That can be then reduced to 250 mcg a day for maintenance.
It is usually paired with tb-500, look up wolverine stack and you’ll get some info on that. Bpc increases blood flow to injured tissues, while tb-500 relieves general inflammation resulting from the injury.
1 Like
Neo
#70
New paper
Diminished signaling via insulin/insulin-like growth factor-1 (IGF-1) axis is associated with longevity in different model organisms. IGF-1 gene is highly conserved across species, with only few evolutionary changes identified in it.
This study investigated the whole exome sequencing data from 2,108 individuals in a cohort of Ashkenazi Jewish centenarians, their offspring, and controls without familial longevity to identify functional IGF-1 coding variants. We identified two likely functional coding variants IGF-1:p.Ile91Leu and IGF-1:p.Ala118Thr in our longevity cohort.
Consequently, diminished IGF-1 signaling resulting from these variants may contribute to exceptional longevity in humans.
Given the previously identified role of reduced insulin/IGF-1 signaling in models of longevity, our findings provide additional evidence for the potential role of these gene variants and reduced IGF-1 signaling in human longevity.
Understanding the mechanisms of rare longevity-associated variants found in individuals with exceptional longevity is of paramount importance in advancing our knowledge of how genes that carry these variants regulate downstream signaling of pro-longevity pathways and could serve as promising gerotherapeutic drug targets.
a recent large-scale study involving nearly 450,000 UK biobank participants showed that older adults with higher IGF-1 levels had greater risk of mortality and age-related diseases, indicating that lower IGF-1 levels were beneficial for their survival55. In our longevity cohort, carriers of IGF-1:p.Ala118Thr had significantly lower levels of IGF-1, compared to non-carriers (Fig. 1B).
https://www.nature.com/articles/s41598-025-94094-y#Fig1
featured at the top here:
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How often do you measure your IGF-1 level?
