19 replies to this topic

[greenleaf]

r-igf1 had clinical studies showing that it can produce small increases in muscle mass. lr3 igf-1 has never had a single clinical study done. it was shown to be harmeful and cause kidney faliure in mice so i seriously doubt human testing will ever be done. rIGF-1 definatly produces muscle tissue but there is no way in he11 that LR3 IGF-1 does. i consider it a waste of money and a joke and i gurentee that i will never see one single piece of info proving me wrong

[Thinkbig]

r-igf1 had clinical studies showing that it can produce small increases in muscle mass. lr3 igf-1 has never had a single clinical study done. it was shown to be harmeful and cause kidney faliure in mice so i seriously doubt human testing will ever be done. rIGF-1 definatly produces muscle tissue but there is no way in he11 that LR3 IGF-1 does. i consider it a waste of money and a joke and i gurentee that i will never see one single piece of info proving me wrong

OK, I THOUGHT I UNDERSTOOD YOU RIGHT.

THATS AN INTERESTING POINT, AND A GOOD ONE TO BRING UP.

I'D LIKE TO GET SOME FEEDBACK ON IGF LONG SPECIFICALLY FROM THE EXPERTS.

I WISH N4CER WAS STILL ROUND THESE PARTS.

[\SHINE/]

r-igf1 had clinical studies showing that it can produce small increases in muscle mass. lr3 igf-1 has never had a single clinical study done. it was shown to be harmeful and cause kidney faliure in mice so i seriously doubt human testing will ever be done. rIGF-1 definatly produces muscle tissue but there is no way in he11 that LR3 IGF-1 does. i consider it a waste of money and a joke and i gurentee that i will never see one single piece of info proving me wrong

Interesting, I've seen so many varing opinions on IGF and studies lately it would be nice to get some solid facts for sure.
I would also like to see some hard core evidence on the LR-3 type.

for now here's another study on IGF-I



Lynch GS, Cuffe SA, Plant DR, Gregorevic P. IGF-I treatment improves the functional properties of fast- and slow-twitch skeletal muscles from dystrophic mice. Neuromuscul Disord. 2001;11(3):260-8.

ABSTRACT

Although insulin-like growth factor-I (IGF-I) has been proposed for use by patients suffering from muscle wasting conditions, few studies have investigated the functional properties of dystrophic skeletal muscle following IGF-I treatment. 129P1 ReJ-Lama2(dy) (129 ReJ dy/dy) dystrophic mice suffer from a deficiency in the structural protein, laminin, and exhibit severe muscle wasting and weakness. We tested the hypothesis that 4 weeks of IGF-I treatment ( approximately 2 mg/kg body mass, 50 g/h via mini-osmotic pump, subcutaneously) would increase the mass and force producing capacity of skeletal muscles from dystrophic mice. IGF-I treatment increased the mass of the extensor digitorum longus (EDL) and soleus muscles of dystrophic mice by 20 and 29%, respectively, compared with untreated dystrophic mice (administered saline-vehicle only). Absolute maximum force (P(o)) of the EDL and soleus muscle was increased by 40 and 32%, respectively, following IGF-I treatment. Specific P(o) (sP(o)) was increased by 23% in the EDL muscles of treated compared with untreated mice, but in the soleus muscle sP(o) was unchanged. IGF-I treatment increased the proportion of type IIB and type IIA fibres and decreased the proportion of type I fibres in the EDL muscles of dystrophic mice. In the soleus muscles of dystrophic mice, IGF-I treatment increased the proportion of type IIA fibres and decreased the proportion of type I fibres. Average fibre cross-sectional area was increased in the EDL and soleus muscles of treated compared with untreated mice. We conclude that IGF-I treatment ameliorates muscle wasting and improves the functional properties of skeletal muscles of dystrophic mice. The findings have important implications for the role of IGF-I in ameliorating muscle wasting associated with the muscular dystrophies.


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[\SHINE/]

http://www.pubmedcentral.nih.gov/articlere...p;artid=1187088

Again another study suggest that IGF-1 and GH when taken together are synergistic as they both have slightly different growth action mechanisms.. like the study above seems to suggest.. IGF-1 has a more localized effect, sometimes working as a paracrine hormone.



problem is IGF-I has only been studied in an endocrinology/physiology perspective, rather than a bodybuilding perspective. I guess what all of us are doing, is pretty much trying to bring the two perspectives together.

Peace.

[\SHINE/]

Interesting, I got this from a good friend who e-mailed this doc.
Peace.

From a world authority in igf studies



In reply to your question, there are no studies in man to the best of my knowledge (LR3 IGF1). Some of the IGF-I analogues have been found to be potent mitogens.

We are at present performing a worldwide survey on the prevalence of malignancy in patients with IGF-I deficiency and their family relatives.

Best regards,

Zvi Laron, MD
_______________________
Prof. Zvi Laron
Endocrinology and Diabetes Research Unit,
Schneider Children's Medical Center
Petah-Tikva 49202
Israel


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for binding facts:

Differences in the association of insulin-like growth factor-I (IGF-I) and IGF-I variants with rat, sheep, pig, human and chicken plasma-binding proteins.

Lord AP, Bastian SE, Read LC, Walton PE, Ballard FJ.

Child Health Research Institute, North Adelaide, South Australia.

"Associations between labelled insulin-like growth factors (IGFs) and IGF-binding proteins in plasma have been compared in the rat, sheep, human, pig and chicken. The IGFs tested were recombinant human IGF-I, the truncated variant, des(1-3)IGF-I, and LR3IGF-I, an extended form that had been engineered so as to minimize interactions with IGF-binding proteins. Marked species differences were demonstrated, notably that the IGF-I variants which exhibited extremely weak binding in rat plasma bound significantly in plasma from the other species. This result was shown both by size-exclusion chromatography of labelled IGFs added to plasma, in which the extent of variant IGF-I binding decreased in the order sheep > human > pig = chicken > rat, and by competition for labelled IGF-I binding in vitro, in which the order was pig = chicken > sheep > human > rat. Notwithstanding these differences, the two IGF-I variants showed only slight between-species binding differences when tested with purified rat, sheep and human IGF-binding protein-3. Ligand blotting experiments with plasma from the five species similarly showed a consistent pattern in that IGF-I binding was much greater than des(1-3)IGF-I binding, which in turn was greater than LR3IGF-I binding"

less binding,more powerful.