#33

I think I’ll try ipamorelin and CJC-1295. Peptides are great. I’m glad to have discovered them.

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#34

I’m happy with the results so far :slight_smile:

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#35

Hi Steve,

You seem to have deep knowledge of peptides, especially regarding those telling the body to secrete GH. Are you able to share details of your supplier?

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#36

A pre-print:

Isolating the Direct Effects of Growth Hormone on Lifespan and Metabolism

Prior studies show that disrupting somatotropic axis components extends laboratory mouse lifespan, but confounding effects of additional genes and hormones obscure the specific impact of growth hormone (GH) on longevity. We address this issue by using mice with a specific knockout of the GH gene, revealing that disrupting GH alone substantially increases lifespan. The longevity effects are accompanied by altered metabolic fuel utilization, directly linking GH action to aging mechanisms.

https://www.biorxiv.org/content/10.1101/2024.09.18.613718v1?ct=

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#37

I’m wondering about this approach about blocking IGF-1 and GH is a bit uni dimensional approach, you will always need it in your brain and tissues to split and regenerate from the stem cells i dont want to live to 200 yo with reduced intelligence,brain mass or weak body. Even the estrogens or E5 and the pig brain drive growth factors are based on growth approach ( look for estrogens and thier interactions with the IGF1 receptors in the brain ):thinking: so i guess fighting Senescence , rapa for the immunity and cancer early-ish detection and mitigation is the way with keeping that GH side optimal :yin_yang:

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#38

There is data that suggests that the IGF-1 inhibition (for healthy lifespan extension) may be something that provides the vast majority of its benefit if done early in life. Its not clear to me if it provides much value later in life. Perhaps (like most of these things) its better on a pulsed dosing schedule.

Past discussions on this topic:

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#39

Longer fasts also increases testosterone while the Gh
Subsides after a few days. The key might be not to overdo longer fasts, finding sweet spot is challenging though.

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#40

Old post but did 75mg DHEA jack up heart rate and raise blood pressure? That seems like a lot

#41

I’m not sure on the heart rate thing as we take the DHEA the same time we take our night time Ipa+CJC stack and that alone increases heart rate a bit.

I picked 75mg as it seems to be middle ground between 50 and 150 as acceptable/safe doses. Some people dose as high as 200mg but I would not be comfortable with that. A friend tried the 75mg and found it made him “angry” so he stopped and became his old lovable self shortly after.

The effect of six months treatment with a 100 mg daily dose of dehydroepiandrosterone (DHEA) on circulating sex steroids, body composition and muscle strength in age-advanced men and women

1 Like
#42

I noticed very elevated heart rate when I went from 25mg to 50mg as it took me to way above physiological range of DHEA-S level

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#43

I find that with most things I’m what I’d call a low to moderate responder as far as noticeable effects.

I often get asked “how did you feel when you took XYZ?” and rarely do I “feel” much of anything. I’d love to be able to do more testing but for now I’d rather put that money into some else LoL!

I suck at being a good guinea pig other than I’m “in” when “it” looks intriguing…

#44

Rapamycin inhibits the downstream effects of IGF-1, and IGF-1 rescued rapa-induced growth inhibition, so there is an interplay between rapa and IGF-1.
IGF-1 rescues rapamycin-induced cell growth inhibition

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#45

The article believes that the inhibition of part of the downstream signaling (the mTOR - 4E-BP1. axis) is bypassed. However it is an oldish article (2006), I wonder if the topic has been explored further by other authors.

The rescue of p-4E-BP1 despite complete inhibition of mTOR-raptor kinase activity supports the existence of non-mTOR inputs to 4E-BP1.

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#46

Growth hormone–deficient Ames dwarf mice resist sarcopenia and exhibit enhanced endurance running performance at 24 months

Ames dwarf mice (df/df) live 50% longer than normal littermates due to a genetic defect in growth hormone (GH) signaling. The enhanced longevity of Ames dwarfs has been studied extensively in an endocrinological context of cellular metabolism and increased resistance to oxidative stress (Bartke. World J Mens Health 37(1):19, 8; Bartke 2; BartkeJ Am Aging Assoc 23(4):219, 10; Bartke. World J Mens Health 39(3):454-465, 11; Brown-Borg et al. Nature 384(6604):33-33, 1; Masternak et al. 2018). However, the skeletal muscle system is relatively unexplored, the quality of which dictates metabolic homeostasis, permits movement and exercise, and exerts paracrine effects on other organs (Delmonico and Beck Am J Lifestyle Med 11(2):167-181, 25; Evans et al. GeroScience 46(1):183, 26; Kim and Kim. Endocrinol Metab (Seoul) 35(1):1-6, 15; Masternak et al. 2018).

Here, we characterize the fitness capacity and skeletal muscle morphology of Ames mice to determine if previously established longevous effects of GH deficiency extend to skeletal muscle tissue. Mutually exclusive, age-matched cohorts of male Ames mice and wildtype controls performed grip strength, rotarod, and endurance running experiments over 6 months. The largest difference in physical performance was observed in endurance running capacity, where dwarf mice outperformed wildtype controls increasingly with age. Tibialis anterior (TA) muscles were evaluated for myofiber size, quality, and environment. Ames mice show reduced myofiber cross-sectional area (CSA) paired with increased myofibers per muscle. Dwarf myofiber populations are less heterogenous in size and seemingly resist sarcopenia, as skeletal muscle from aged individuals shows youthful morphological resemblance in mean myofiber CSA, size frequency distribution, and presence of fibrotic tissue. Declines in fitness performance and myofiber integrity were observable in age-matched wildtype controls. Utilizing an established longevity model to investigate skeletal muscle function and morphology is a novel approach to gaining insight into the seemingly inverse relationship between GH signaling and mammalian longevity.

Open access paper:

3 Likes
#47

While that may be the case with mice, personally I’m a bit more interested in having strong tendons and ligaments.

Since BPC 157 stimulates hGH receptors in ligaments and tendon, in humans, and having a more “youthful” level of hGH at the “right” time could help maintain and possibly strengthen my old man connective tissues. So I’m willing to trade a bit of “longevity” for strength.

Abstract

Tendon collagen content and circulating growth hormone (GH) are reduced in elderly. In a placebo-controlled, double-blinded study, we examined if local injections of rhGH enhance collagen synthesis in healthy elderly men (61 ± 1 yr). Two injections of rhGH or saline (control) were injected into each of the patient’s patellar tendons, respectively. Subsequently, tendon collagen fractional synthesis rate (FSR) and an indirect marker of type I collagen synthesis (PINP) were measured.

https://journals.physiology.org/doi/full/10.1152/japplphysiol.00816.2012
s4

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#48

Me too. I want to run for five more years, and I don’t care what happens after that.

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#49

In his study of centenarians Nir Barzilai found that many centenarians had a mutation that hindered the cell’s ability to take up IGF. Sounds consistent with the finding that centenarians tend to be smaller (catabolic?) – and in the extreme, tiny (Laron dwarves). The extreme end of the catabolic spectrum.

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#50

Good thing you are probably getting both longevity and strength

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#51

But is that what happens or are you trading more strength now for less strength further in the future?

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#52

But the results were not statistically significant - and the results they looked at were only hours after the stimulation and not if the tendons actually became healthier and stronger?

2 Likes