feedback by biochemist about IGF from research corp.

[tk...]

Interesting IGF info - Makes me think twice about ordering from Research companies.

Ok, I got this from the muscletalk forums. I thought it was real interesting..

''here is some info written by MuscleTrainee......worth reading

I feel like I ought to offer some more thoughts, with respect to IGF-1.

I begin by saying that I've used the stuff on myself, under several different regimens. But, more importantly, I've now worked with quite a number of other athletes, using IGF-1. In these situations, I've had control over the dosage, administration, and diet. And I've prepared the IGF-1 injectable under standardized conditions, using appropriate buffers. I would receive regular reports and observations from the users. While I do not consider my data to have a sample size which would stand a test of statistical validity, my data base is larger and better quality than the individual anecdotal observations seen in board threads.

There are a tremendous number of issues, not directly related to IGF response, and I'll discuss them, first.

There are a number of boards which are seen as authorities for good information, yet are polluted by members and mods who are directly connected with IGF dealers. Furthermore, there are buyers who have been induced to act as shills. These people never identify their roles, and they have completely muddied the waters with their hype and outright lies. For example, I know of one guy who is an IGF powder middleman, and he has managed to get himself known as an IGF "expert", even though he has absolutely no science background. He goes around from board to board belching out some of the most absurd hype I've ever seen, all the while hustling people to buy their IGF from the company he sells his powder to.

Then there are the ones who have some decent knowledge, but have gotten their knowledge all mixed up. In that thread cited, above, from the Cutting Edge Muscle board, one member posts about how good he thinks IGF is, then he offers a proposed ideal diet for maximizing the effect of IGF. Well, if you look at that diet, you will realize that you can do that diet, and put on 5-6 pounds easy, and not use any IGF-1! It's the diet that is making you grow, not the IGF!! Just ridiculous!!! Anyone should be able to see through that sort of nonsense, yet IGF is seen as such a "Holy Grail", that things like this are overlooked.

Another class of post is by those who don't fully understand what is happening, when they use IGF-1. Yes, some legit research has shown that IGF can multiply muscle fiber. But it is clear to me that the bulk of the response to IGF comes from it's ability to act as a sensational glucose disposal agent. This is the part where IGF's name, "Insulinlike", comes to the fore. IGF can send you into ketosis with ease. Good responders to IGF are hungry all the time, because the blood glucose is held low. All that glycogen is being driven into the muscles. The frequent reports of muscle fullness and vascularity is the result of muscles being pumped full of glycogen and water.

There is too little mention of the non-responders to IGF-1. They definitely exist. But identifying the percentage of them in the population is difficult, due to the way most IGF is being sold. I'll discuss that, next.

The business is rife with misinformation on how to properly prepare the IGF-1 for use. The ONLY proper way to rehydrate IGF-1 for use, where it will be at full strength and activity, is with an aqueous buffer solution, which has the proper pH and ionic(salt) content. However, it is not easy or safe for the average user to prepare such a buffer, and access to the raw materials is limited.

A couple of years ago, Animal concocted the idea of dissolving the IGF he was selling, in some BA. He perhaps did not have access to the proper buffer materials, and he came up with this idea, in order to promote his business. Well, it sort of worked. But some, if not most, of the IGF is rendered useless by this method, since you need the correct pH and ionic environment for the peptide chains to unwind. In the end, you have to use a lot of IGF, just to get the effect which you would get, if you had properly rehydrated it with a buffer. In my work, using a proper buffer, the maximum dosage per day is 30 mcg. But I've seen good results on only 15 to 20 mcg's per day. It is typical for users with the Animal type product to have to use 50 to 120 mcg per day, to see any effect at all.

Still another absurd notion is that you do not have to refridgerate the IGF in BA. I have seen some idiot "experts" recommend that "IGF-1 works better if you store it in your sock drawer".

Now, I'm a chemist, and I've worked in biochem labs, and seeing all this online nonsense about preparing IGF really makes me crazy. But, let's use a little common sense. Both IGF-1 and hGH are chain sequenced peptides. So, they are in the same family. Now, we all know that you rehydrate GH with an aqueous solution and we must store it under refridgeration. Yet, these "experts" say we can reconstitute IGF-1 with BA and it does not require any refridgeration. I ask you, have any of you ever seen anyone recommend that we reconstitute GH with BA, and that we not store it under refridgeration? I certainly never have. It seems to me that this would be a real breakthrough, right? Not a single legit biochemist has ever advocated the BA method for preparing chain sequenced peptides. Again, I have never seen one of these online "experts" advocate using BA for preparing GH, yet GH and IGF-1 are in the same family. Now, doesn't that tell you something??

So, you may begin with some active IGF in these BA preparations, but you end up with less and less, as it degrades.

Then there is the shipping. Ever wonder why we don't buy hGH in reconstituted form? Aside from having to keep it cold, all the shaking and agitation, which goes on in shipping and transportation, would destroy the peptide chains. Yet these "experts" say there's no problem in selling and transporting IGF-1 in liquid form. Are we to believe that BA creates some wondrous, new, indestructable environment for peptide chains?

So, now we go a step further. We begin with some active IGF in the BA preparation, but it degrades, and then we ship it, and then we lose still more and more.

By the time you end up with it, in your hands, there is little or no active IGF-1. So, now, how do we determine who is a IGF non-responder, and who simply has gotten a ruined bottle of IGF-1? How do we determine the full range of response in the population, when the IGF-1 in the field is of random strength and unknown concentration?

All these problems make a complete assessment of the true worth of IGF-1 very difficult. The buyer thinks he has 1000 mcg per ml of IGF-1, when, in reality, he has much less, maybe even none.

It is my contention that much of the weight gain, seen by IGF-1 users, is water. Their muscles appear to be growing, but it is glycogen and water. Some will respond in extreme. I had one user put on almost 15 pounds. All water! Three days after his IGF cycle ended, the water was gone, and so was the weight gain. So, we are mostly seeing bloat, to a greater or lessor degree, rather than spectacular muscle growth. This accounts for all the stories of giant pumps, while training on IGF-1.

I'm not convinced that there is really significant muscle growth. But I am convinced that there is bodyfat loss. As I mentioned, if your carbs are low enough, IGF-1 will get you into ketosis quickly, and then bodyfat loss will proceed accordingly.

IGF-1 is not useless. IGF-1 is, at present, a very specialized tool. I think it's best use comes with bulking. Through its very powerful glucose disposal effect, a responder is always hungry, and the nutrition is pumped into the muscles. People who have difficulty eating while bulking, may find that they have fewer problems packing in that food. But, if you're an ectomorph, that will result in a much greater food demand, since you will need to eat more to compensate for the loss in blood glucose. You will most certainly have to eat in the middle of the night, due to hunger.

IGF-1 is also useful while cutting, but it really makes you crave carbs, and, if you're not interested in going keto, then you end up having to eat more carbs than you would, otherwise. The glycogen pumping effect is anti catabolic, however.

But that's about it, as far as I'm concerned.

If you are to make the best use of IGF-1, then the preparation of the buffer will be a serious handicap. The starting materials are not easy to obtain, and the handling and storage of these chemicals is dangerous and difficult. If you prepare the buffer with the wrong pH, then you will completely destroy the IGF-1, the moment you add it to the buffer. You better know what you are doing, and have the correct equipment with which to do it.

There are so many more cost effective and productive ways to spend your money on muscle building, than with IGF-1. If you're adventurous, done plenty of research, and have a wad of cash, then go ahead and give it a try. But IGF-1 is not the Holy Grail of bodybuilding.

Have fun!''

Hmm, after reading this, I'm thinking that maybe the best way to get IGF would be in powder form and add the BA yourself? That way it would last longer right? Or is it not that simple?
Any idea's or comments?
Hope you liked the article bro's

 

[Mudge]

Originally posted by tk...
Well, if you look at that diet, you will realize that you can do that diet, and put on 5-6 pounds easy, and not use any IGF-1

Oy vey. If people actually made all their gains from the drugs without changing their diets then they would lose it all when they came off. The difference here is, if you can put on the weight naturally it is not likely to be as much muscle as if you are cycling an anabolic, "duh."

Now I am around 600 calories a day less than my last cycle and I am down 6-8 pounds from where my peak was, and I plan to lose more bodyweight than that (yes on purpose).

Just wanted to bring that up, back to reading the article.

 

[Mudge]

Originally posted by tk...
Hmm, after reading this, I'm thinking that maybe the best way to get IGF would be in powder form and add the BA yourself? That way it would last longer right? Or is it not that simple?

Read it again

 

[tk...]

i just received my IGF in Ba two weeks ago, since then i have refrigerated it. I havent started shooting yet due to my illness, but now that i have finished my antibiotics, i wonder how much active IGF is left in the vial .......

to compensate, am gonna have to increase to dosage from 20 mcg/day to 40 mcg/day which would last me 25 days instead of 50.


mudge, your probably right, the best way would be in powder form. I have no experience whatsoever with BA solutions, but if creating a buffer is a must, then i personally know that this is no easy task simply because you require the right equipment. I would have to reconstitute it at my university.....

 

[Mudge]

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 aren???t spectacular. More often than not, they don???t even come close to gains seen using androgens.

For the most part, people should realize that IGF-1 is primarily responsible for GH???s 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, I???m 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 can???t 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 don???t 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, you???re providing the catalyst for cancer formation, so to speak. Let???s say, for instance, you get many sunburns during your lifetime. Now, let???s say that one cell has its DNA damaged or altered. This, in and of itself, isn???t 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, let???s 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 won???t 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 don???t 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, you???re 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, I???m actually referring to Long R3 IGF-I as it???s 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 you???re 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. It???s 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)

References Cited

1. Tuzcu A, et al. "Insulin sensitivity and hyperprolactinemia." J Endocrinol Invest. 2003 Apr;26(4):341-6

2. Freemark M, et al. "Body weight and fat deposition in prolactin receptor-deficient mice." Endocrinology. 2001 Feb;142(2):532-7

3. Wasada T, Kawahara R, Iwamoto Y. "Lack of evidence for bromocriptine effect on glucose tolerance, insulin resistance, and body fat stores in obese type 2 diabetic patients." Diabetes Care. 2000 Jul;23(7):1039-40

4. Pijl H, et al. "Bromocriptine: a novel approach to the treatment of type 2 diabetes." Diabetes Care. 2000 Aug;23(8):1154-61

5. Ohem N, Holzl J. Some new investigations on Ilex paraguariensis - Flavonoids and triterpenes. Planta Med 1988; 54: 576

6. Bisset NG, ed. Herbal Drugs and Phytopharmaceuticals (Wichtl M, ed., German edition). Stuttgart: Medpharm, 1994

7. Duke JA. Handbook of Medicinal Herbs. Boca Raton: CRC, 1985

8. Martindale: The Extra Pharmacopoeia, 29th edn. (Reynolds JEF, ed.). London: The Pharmaceutical Press, 1989

9. The Merck Index. An Encyclopedia of Chemicals, Drugs and Biologicals, 11th edn. Rahway, NJ: Merck, 1989

10. Carani C, et al. "Role of oestrogen in male sexual behaviour: insights from the natural model of aromatase deficiency." Clin Endocrinol (Oxf). 1999 Oct;51(4):517-24

11. Scordalakes EM, Imwalle DB, Rissman EF. "Oestrogen's masculine side: mediation of mating in male mice." Reproduction. 2002 Sep;124(3):331-8

12. Brady BM, et al. "Demonstration of progesterone receptor-mediated gonadotrophin suppression in the human male." Clin Endocrinol (Oxf) 2003 Apr;58(4):506-12

13. Bauer ER, et al. "Characterisation of the affinity of different anabolics and synthetic hormones to the human androgen receptor, human sex hormone binding globulin and to the bovine progestin receptor." APMIS. 2000 Dec;108(12):838-46

14. Markiewicz L, Gurpide E. "Estrogenic and progestagenic activities of physiologic and synthetic androgens, as measured by in vitro bioassays. Methods Find Exp Clin Pharmacol. 1997 May;19(4):215-22

15. Breithaupt-Grogler K, Niebch G, Schneider E et al: Dose-proportionality of oral thioctic acid - coincidence of assessments via pooled plasma and individual data. Eur J Pharm Sci 1999; 8(1):57-65

16. Hermann R, Niebch G, Borbe HO et al: Enantioselective pharmacokinetics and bioavailability of different racemic alpha-lipoic acid formulations in healthy volunteers. Eur J Pharm Sci 1996; 4:167-174

17. Gleiter CH, Schug BS, Hermann R et al: Influence of food intake on the bioavailability of thioctic acid enantiomers. Eur J Clin Pharmacol 1996; 50(6):513-514

18. Fachinformation: Pleomix-Alpha(R), alpha-Liponsaeure. Illa Health Care GmbH, Geretsried, 1996

19. Streeper RS, Henriksen EJ, Jacob S et al: Differential effects of lipoic acid steroisomers on glucose metabolism in insulin-resistant skeletal muscle. Am J Physiol 1997; 273(1 pt 1):E185-E191

20. Khamaisi M, Potashnik R, Tirosh A et al: Lipoic acid reduces glycemia and increases muscle GLUT4 content in streptozotocin-diabetic rats. Metabolism 1997; 46(7):763-768

21. Henriksen EJ, Jacob S, Streeper RS et al: Stimulated by alpha-lipoic acid of glucose transport activity in skeletal muscle of lean and obese Zucker rats. Life Sci 1997; 61(8):805-812

22. Wickramasinghe SN & Hasan R: In vitro effects of vitamin C, thioctic acid and dihydrolipoic acid on the cytotoxicity of post-ethanol serum. Biochem Pharmacol 1992; 43(3):407-411

23. Dimpfel W, Spueler M, Pierau F-K et al: Thioctic acid induces dose-dependent sprouting of neurites in cultured rat neuroblastoma cells. Dev Pharmacol Ther 1990; 14(3):193-199

24. Prehn JHM, Karkoutly C, Nuglisch J et al: Dihyrolipoate reduces neuronal injury after cerebral ischemia. J Cereb Blood Flow Metab 1992; 12(1):78-87

25. Burkart V, Koike T, Brenner HH et al: Dihydrolipoic acid protects pancreatic islet cells from inflammatory attack. Agents Actions 1993; 38(1-2):60-65

26. Bauer A, Harrer T, Peukert M et al: Alpha-lipoic acid is an effective inhibitor of human immuno-deficiency Virus (HIV-1) replication. Klin Wochenschr 1991; 69(15):722-724

27. Suzuki YJ, Aggarwal BB & Packer L: alpha-Lipoic acid is a potent inhibitor of NF-kappaB activation in human T cells. Biochem Biophys Res Commun 1992; 189(3):1709-1715

28. Bierhaus A, Chevion S, Chevion M et al: Advanced glycation end product-induced activation of NF-kappaB is suppressed by alpha-lipoic acid in cultured endothelial cells. Diabetes 1997; 46(9):1481-1490

29. Constantinescu A, Tritschler H & Packer L: alpha-Lipoic acid protects against hemolysis of human erythrocytes induced by peroxyl radicals. Biochem Mol Biol Int 1994; 33(4):669-679

30. Greene EL, Nelson BA, Robinson KA, Buse MG. "alpha-Lipoic acid prevents the development of glucose-induced insulin resistance in 3T3-L1 adipocytes and accelerates the decline in immunoreactive insulin during cell incubation." Metabolism 2001 Sep;50(9):1063-9

31. Maddux BA, et al. "Protection against oxidative stress-induced insulin resistance in rat L6 muscle cells by mircomolar concentrations of alpha-lipoic acid." Diabetes 2001 Feb;50(2):404-10

32. Weinstein RB, Tritschler HJ, Henriksen EJ. "Antioxidant alpha-lipoic acid and protein turnover in insulin-resistant rat muscle." Free Radic Biol Med 2001 Feb 15;30(4):383-8

33. Yaworsky K, Somwar R, Ramlal T, Tritschler HJ, Klip A. "Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by alpha-lipoic acid in 3T3-L1 adipocytes." Diabetologia 2000 Mar;43(3):294-303

34. Jacob S, et al. "Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial." Free Radic Biol Med 1999 Aug;27(3-4):309-14

35. Estrada DE, et al. "Stimulation of glucose uptake by the natural coenzyme alpha-lipoic acid/thioctic acid: participation of elements of the insulin signaling pathway." Diabetes 1996 Dec;45(12):1798-804

36. Hundal RS, et al. "Mechanism by which metformin reduces glucose production in type 2 diabetes." Diabetes 2000 Dec;49(12):2063-9

37. Anderwald C, et al. "Inhibition of glucose production and stimulation of bile flow by R (+)-alpha-lipoic acid enantiomer in rat liver." Liver 2002 Aug;22(4):355-62

38. Saengsirisuwan V, Perez FR, Kinnick TR, Henriksen EJ. "Effects of exercise training and antioxidant R-ALA on glucose transport in insulin-sensitive rat skeletal muscle." J Appl Physiol 2002 Jan;92(1):50-8

39. Evans JL, Goldfine ID. "Alpha-lipoic acid: a multifunctional antioxidant that improves insulin sensitivity in patients with type 2 diabetes." Diabetes Technol Ther 2000 Autumn;2(3):401-13

40. Saengsirisuwan V, Kinnick TR, Schmit MB, Henriksen EJ. "Interactions of exercise training and lipoic acid on skeletal muscle glucose transport in obese Zucker rats." J Appl Physiol 2001 Jul;91(1):145-53

41. Konrad T. "alpha-Lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes." Diabetes Care 1999 Feb;22(2):280-7

42. Jacob S, et al. "Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid." Arzneimittelforschung 1995 Aug;45(8):872-4

43. Jacob S, Rett K, Henriksen EJ, Haring HU. "Thioctic acid???effects on insulin sensitivity and glucose-metabolism." Biofactors 1999;10(2-3):169-74

44. Jacob S, Henriksen EJ, Tritschler HJ, Augustin HJ, Dietze GJ. "Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid." Exp Clin Endocrinol Diabetes 1996;104(3):284-8

45. Bigsby RM, Caperell-Grant A, Madhukar BV. "Xenobiotics released from fat during fasting produce estrogenic effects in ovariectomized mice." Cancer Res. 1997 Mar 1;57(5):865-9

46. McCurdy CE, Davidson RT, Cartee GD. "Brief calorie restriction increases Akt2 phosphorylation in insulin-stimulated rat skeletal muscle." Am J Physiol Endocrinol Metab. 2003 Oct;285(4):E693-E700.

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

 

[tk...]

whoa!!!!! ...i had never seen that post before.
But like we all know, everything causes cancer. Any type of outside source of test. will cause the prostate to enlarge allong with the potencial of prostate cancer, hell, staying in the sun for long periods of time will also cause skin cancer.
Creatine has also been shown to cause cancer as well.

everything causes cancer!!!

although a very interesting post, it wont stop me from shooting.

off topic, i have 1 ml solution of IGF RL3 in BA. Am gonna shoot 40 mcg a day after workout, but i dont know on how much BW i should draw from the vial to dilute the IGF, would anybody know how much?? ,

 

[Mudge]

Well you are born with cancer cells in you (although cells can be damaged and become "cancerous"). So really while it may even stimulate them it wont cause it I'd say, just posting an article is all.

1/25th of a cc bro, thats 4 units (tick marks) on a 1cc slin pin, the first big line should say 10, then 20 and up to the full 1cc, so you want 4 units underneath the 10 line.