People use to call it the fountain of youth at one time. Now there is experts who say the opposite and some say things different than that. Human Grade is always the best IMO. If I could afford it, I would take Genotropin. I never gain water weight from it, but then again, I was not taking very high doses either. I mention I like cycling it on and off too.
Now I am not an expert by no means, but this is what I feel from experience. GH does make you feel younger, but there is a fine line with that. When taking GH, you really need to monitor some things. Like Thyroid levels and sugar to start.
In older adults GH will decrease over the years. So taking GH when you are older will yield different effects than someone who is a lot younger. Taking test does the same, however there is a fine line and abuse will not give the same benefits of HRT in many aspects, health being the front runner.
post from datbtrue:
Certain tumors hi-jack the cellular machinery and secrete GH or IGF-1 and use it to grow and break existing boundaries into other tissue. The cutting edge research is in antagonists for GH, for GHRH, for IGF-1.
What they found is that designing highly specific ligands that bind to GH-receptors in the cancerous tissue in such a way as to block them, results in tumor shrinkage. They are taking away the tumors ability to grow...
Often the tumor shrinks to such a degree that chemotherapy can then be used to eliminate the cancer. These two therapies have proven very effective in all types of cancers even hard to reach lung & brain. The trick is in making delivery vehicles that will target the cancerous region rather then all the other tissue in the body.
The best clinical studies were breast cancer studies which demonstrated total remissions after the use of both therapies. This of course was for the types of cancers that behave as described herein.
Life extension studies using calorie restriction or EOD fasting has demonstrated (so many things) but one is that such states reduce circulating IGF-1. You see the part that is deadly ...the part that reduces life span ...the part that can result in cancers is the intracelluar events that slowly accumulate damage. A fuller explanation & illustrations can be found in my thread at: A complete understanding of IGF-1 & its potential influence on cancer & longevity
I see so many times a post where someone states "IGF-1 can not cause cancer it can only make it grow if it already exists". It makes people feel better to say such things I suppose...
...but a statement like that hints not one bit at understanding that their are states know as pre-cancerous states occurring routinely in our bodies. Many times a tumor suppressor such as P53 will be able to act and shutdown the cell before such states become cancerous. There are a great many factors that operate in our body...
...one theory is that cancers happen fairly routinely and our body often destroys them before they become serious.
Flooding the body with high levels of IGF-1 could conceivably give enough early fuel to these states so as to overwhelm our routine defenses.
Anyway...
IGF-1 LR3 is obviously risky....there are no concurrent binding protein checks.
IGF-1 created naturally (from GH's effects) also comes with an increase in binding proteins which will control how IGF-1 is to be used that is less risky.
Large amounts of GH which sustain high levels of IGF-1 are more dangerous then low "youthful replacement" doses. In fact high levels of circulating IGF-1 is positively correlated with cancer incidence.
Probably, natural pulse creation or increase in tone (i.e. release profile) from GHRPs & GHRH will be the least dangerous at low/mod doses.
Figure 3 think really helps us understand "how IGF-1 can increase cancers".
Figure 3. Model of the influence of insulin -like growth factor 1 signalling on the stepwise accumulation of somatic-cell genetic damage in carcinogenesis. The model of stepwise accumulation of genetic damage leading to carcinogenesis can be extended to include influences of insulin-like growth factor 1 (IGF1) signalling. These include favouring cellular proliferation over arrest and cellular survival over apoptosis. This model provides a preliminary biological framework to account for the observed association of higher levels of IGF1, or IGF1 receptor (IGF1R) activation, with cancer risk in epidemiological and laboratory studies. The model predicts that stepwise accumulation of genetic damage is facilitated in individuals with higher IGF1 levels because in these individuals there is a slightly higher rate of cell division (increasing the risk of errors) and, perhaps more importantly, because the probability of appropriate apoptosis of cells with a small number of 'hits' would be slightly reduced in a microenvironment with higher levels of IGF1R activation. The figure greatly exaggerates the magnitude of the hypothesized differences between 'high IGF' and 'low IGF' individuals in proliferation and apoptosis for purposes of illustration. Very small differences in these parameters, if applied to the very large renewing cell populations of organs such as the colon over a timespan of decades could influence the probability of emergence of a fully transformed clone. Colours indicate the following: yellow, normal cells; pale blue, cells containing one mutation or hit; dark blue, cells containing two mutations or hits; purple, apoptotic cells.
**broken link removed**
Figures
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