Thread: einstein - opinion about IGF-?
06-21-2004, 12:27 PM #1New Member
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einstein - opinion about IGF-?
I'm interested in what you think about Cy Willson's article on IGF-1. While I respect Cy's opinion on some matters, I think he is way off base on others. Where do you think he is here?
Posted on ******:
Intelligent Drug and Nutrition Info
by Cy Willson
"IGF-1: Worst Bodybuilding Drug Ever?
Q: What ever happened to IGF-1? It was talked about in 'roid books in the early '90s but you don't hear much about it now, except for a few sleazy supplement companies who are using the name.
A: IGF-1 can allow for hypertrophy of muscle. Will it do such a thing when administered to humans? Yes. However, the gains seen really arenít spectacular. More often than not, they donít even come close to gains seen using androgens.
For the most part, people should realize that IGF-1 is primarily responsible for GHís anabolic effects in skeletal muscle as well as cell proliferation, leading to enlarged internal organs and increasing the risk for cancer dramatically. Oh, and this most certainly includes Long R3 IGF-I as I know some people will try to argue that it's much safer.
Well, in order to give you the total picture, Iím going to go over some basic molecular biology as well as list the direct evidence we have concerning the side effects of IGF-1 and yes, that includes Long R3 IGF-I.
First, people should understand that in the human cell cycle, growth requires growth factors in general. Seems simple enough. The next thing people need to understand is that for a normal cell, death is something that'll inevitably occur via loss of telomerase or apoptosis (programmed cell death). Again, I canít overemphasize enough that the default pathway in humans is death, not growth. (Reassuring, isn't it?)
Now, when you hear of cancer, malignant cancer, people tend to think of uncontrolled cell division. Essentially though, these transformed cancerous cells are immortalized. Now, many changes are required for this to occur (i.e. increased telomerase, increased bcl-2, increased myc and decreased p53). In the development of cancer, we tend to think of carcingogens consisting of both initiators and promoters. For instance, some initiators are UV radiation and tobacco smoke, usually causing DNA damage or mutation, whereas promoters tend to stimulate cell division. A few examples are phorbol esters, hormones (e.g. estrogens) and yes, growth factors.
Now, keep in mind both events, initiation and promotion, are required for the development of malignant cells. As a side note, viral infection can also lead to the two events, but I digress. Anyhow, normally a cell serves its purpose and then dies via apoptosis. However, malignant cells donít undergo apoptosis. They are, as I said before, immortal. The normal triggers to apoptosis are DNA damage, loss of cell-matrix contact, loss of cell to cell contact, and last but most certainly not least, lack of growth factors.
When you introduce growth factors, youíre providing the catalyst for cancer formation, so to speak. Letís say, for instance, you get many sunburns during your lifetime. Now, letís say that one cell has its DNA damaged or altered. This, in and of itself, isnít too much of a concern as this is only one part of the equation, the iniation. The second part is the promoter (including growth factors).
Well, letís imagine we introduce growth factors to the cell which has damaged or mutated DNA and it then begins to divide at a more and more rapid rate until it wonít stop. Voila , you have a tumor, which is now capable of even faster growth as well as being invasive (able to invade surrounding tissues) and metastatic (able to cause growth in completely unrelated and distant tissues) in regard to other tissues.
In other words, you now have a malignant tumor, which we commonly refer to as cancer. The fact is, cancer stems from just one cell, just one cell, which begins to divide uncontrollably. People often talk about GH and the side effects thereof, but what most donít realize is that many of those side effects aren't necessarily mediated by growth hormone but by IGF-1.
Many people may go their whole lives with some DNA damage (or mutation rather) and never have cancer, but with the addition of growth factors, youíre asking for trouble. Even more specifically, you can increase the risk of developing rare forms of cancer, like sarcomas, which are tumors commonly found in connective tissues (i.e. muscle, bone, cartilage, etc.)
Okay, now on to the more cosmetic side effects. With Long R3 IGF-I, it was shown to stimulate growth of the gastrointestinal tract. IGF-1 actually had no effect on body weight and wet tissue weight of the small and large intestine, whereas Long R3 IGF-I resulted in a 20% increase in the weight of the small and large intestine. This is what's causing a "GH gut" although using Long R3 IGF-I is much, much worse than using GH.
Something else to keep in mind is that Long R3 IGF-I was shown to be even more potent than IGF-1 in inhibiting apoptosis and thus its potential for causing cancer is many times greater.
Another idea is that IGF-1 may also keep telomerase activity high, which as we noted previously is a contributing factor for the loss of regulation in terms of cell division. In other words, it again can substantially increase the risk for developing cancer. Long R3 IGF-I was shown to increase telomerase activity in human prostate cancer cells, whereas IGF-1 had no effect.
So, when I tell you to stay away from IGF-1, Iím actually referring to Long R3 IGF-I as itís what's most commonly circulated and used. Although both aren't something a person should use, Long R3 IGF-1 is probably the worst choice you can make.
So, unless youíre an IFBB pro who consistently places in the top ten at popular contests, you should forget about using IGF-1, or specifically the analogue of IGF-1 called Long R3 IGF-I. Itís really not worth the risk. This, out of all the compounds that bodybuilders may use, is probably the worst in terms of potential side effects.
If you want a true distended belly and increased risk of cancer, be my guest. (47-52)"
47. Steeb CB, Trahair JF, Read LC. "Administration of insulin -like growth factor-I (IGF-I) peptides for three days stimulates proliferation of the small intestinal epithelium in rats." Gut. 1995 Nov;37(5):630-8
48. Wetterau LA, Francis MJ, Ma L, Cohen P. "Insulin-like growth factor I stimulates telomerase activity in prostate cancer cells." J Clin Endocrinol Metab. 2003 Jul;88(7):3354-9
49. Devi GR, Graham DL, Oh Y, Rosenfeld RG. "Effect of IGFBP-3 on IGF- and IGF-analogue-induced insulin-like growth factor-I receptor (IGFIR) signalling." Growth Horm IGF Res. 2001 Aug;11(4):231-9
50. Nickerson T, Huynh H, Pollak M. "Insulin-like growth factor binding protein-3 induces apoptosis in MCF7 breast cancer cells." Biochem Biophys Res Commun. 1997 Aug 28;237(3):690-3
51. Vink-van Wijngaarden T, Pols HA, Buurman CJ, Birkenhager JC, van Leeuwen JP. "Inhibition of insulin- and insulin-like growth factor-I-stimulated growth of human breast cancer cells by 1,25-dihydroxyvitamin D3 and the vitamin D3 analogue EB1089." Eur J Cancer. 1996 May;32A(5):842-8
52. Wetterau LA, Francis MJ, Ma L, Cohen P. "Insulin-like growth factor I stimulates telomerase activity in prostate cancer cells." J Clin Endocrinol Metab. 2003 Jul;88(7):3354-9
06-21-2004, 12:39 PM #2New Member
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Cy Willson is basically saying that IGF-1 will activate the cancer cells and is really dangerous, and LR3 IGF-1 is even more so. In addition, he says that IGF-1 is what is responsible for the GH gut. He also doesn't seem to think it provides that much benefit.
06-21-2004, 12:43 PM #3
06-21-2004, 12:45 PM #4New Member
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Ah, the ol' search engine. I knew you probably had covered it before. My apologies. Thanks.
06-21-2004, 12:46 PM #5
This has already been addressed...do a search. Let us know if you cannot find it. Lot's of good info about IGf-1 here. Peace
06-21-2004, 03:09 PM #6
His article is talking about iGF-1 not LR3 IGF-1 big difference.
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