t-mag.com called IGF-1 worst bb drug ever

[northendninja]

not sure if you guys read this, but im interested in your rebuttals. I know t-mag folks are biased but they have some interesting accusations/points.

sorry, i know, long read:

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)

[einstein1905]

First off, whoever wrote that must have been on the chapter on apoptosis in their undergrad molecular biology class at the time it was written. I see no purpose to preface an article with the rudimentary mechanisms of the development of cancers and then go on to merely speculate (without referencing any literature) how IGF-1 may fit into this picture. They speculate that IGF-1 (but in particular, LR3) may play a role as catalyst in cancers.....yes....we assume so too. It may exacerbate an existing cancer....that is a potential risk. LR3 is simply a more potent version of physiological IGF-1, so its effects are going to be dose-dependent.....adjust for the appropriate dose, and IGF-1 will have similar effects to LR3. The use of AAS (test) has been shown to increase IGF-1 levels substantially, so those that have been using AAS for years, even decades, have been bathing in this cancer-prone environment for years on end......do you see any significant increase in the incidence of cancers among BBers? The same can be said for GH, which has been around for a while (much longer than LR3).
They allude to a few in vitro assays that potentially have some correlational relevance to the real world (however, they neglect to cite them) but lack an real world evidence of their claims.....I'd tip my hat to them if they even had a rodent model experiment showing increased risk of cancers in response to elevated IGF-1 levels (let alone LR3). It's a pretty bold assertion calling IGF-1 the worst BB supplement without any real evidence to support that claim.

As for the lack of aesthetic effects, you need not look any further than some recent threads where users raved about our experiences with LR3.


You can theorize until you're blue in the face, but if it doesn't translate to the real world, it's all just speculation.

[Da Bull]

Excellent retort einstein!

[cpt steele]

Nicely done Einstein

[einstein1905]

In fact here is a study that shows IGF-1 to exacerbate an existing tumor. This is something we all pretty much agree on: GH/IGF-1 is a bad idea if you have cancer of any type
What the article above seems to stress, and w/o just cause IMO, is that IGF-1 has the potential to take a predisposition for cancer and turn it into cancer....there is simply no evidence of that. In most cancers, several mutations must occur before cancer results. There is absolutely no reason to believe IGF-1 plays any role in these mutations. However, if the required mutations do occur (due to genetic predisposition, environmental factors, and mere stochastic probability), then cancer can result. It's at this point that IGF-1 can play a role is promoting preexisting cancerous growth. My point is.....GH/IGF-1 does not increase your risk for cancer....it can, however, take an existing cancer and cause it to progress more rapidly, which, like I said, is nothing new.




Biochem J. 1994 Aug 1;301 ( Pt 3):769-75. Related Articles, Links


Effects of insulin and insulin-like growth factors on protein and energy metabolism in tumour-bearing rats.

Tomas FM, Chandler CS, Coyle P, Bourgeois CS, Burgoyne JL, Rofe AM.

Cooperative Research Centre for Tissue Growth and Repair, Adelaide, Australia.

The effects of insulin-like growth factor-1 (IGF-I), and a more potent variant LR3-IGF-I, which binds poorly to IGF-binding proteins, were investigated in rats bearing a mammary adenocarcinoma. The effect of insulin, either alone or in combination with LR3-IGF-I, was also investigated. Peptides were infused via osmotic minipumps for 6-7 days after tumour size reached 5% of body weight. Infusion of IGFs alone at either 200 or 500 microgram/day significantly decreased food intakes as well as circulating levels of insulin and glucose, and consequently failed to promote muscle protein accretion in the host. Tumour growth was increased by the IGFs, especially by LR3-IGF-I, even though these peptides did not promote growth of the adenocarcinoma in cell culture. Infusion of LR3-IGF-I, and to a lesser extent IGF-I, led to decreased rates of muscle protein synthesis and increased muscle protein breakdown, but each of these measures was closely related to the final tumour burden (r2 = 0.454 and 0.810 respectively; P < 0.01) and possibly resulted from a decrease in substrate supply to the host tissues. Insulin infusion (100 micrograms/day) increased food consumption by more than 50% and significantly decreased tumour growth. Insulin and LR3-IGF-I had a synergistic effect on host weight, which increased by 19.1 +/- 1.9, -1.1 +/- 4.7 and 37.9 +/- 1.5 g for insulin, LR3-IGF-I and combined treatments respectively. Carcass protein was increased by more than 10% with insulin treatment, due to increased rates of synthesis and decreased rates of muscle protein breakdown, but LR3-IGF-I had no positive effect on carcass protein accretion, either alone or in combination with insulin. Similarly, the amount of carcass fat was increased almost 2-fold by insulin treatment, whereas it was decreased by 30% by LR3-IGF-I. These changes may have arisen either from direct hormone effects on metabolism or from the indirect effects of food intake, or both. Our results suggest that IGF administration may exacerbate an insulin insufficiency associated with the tumour-bearing state and further decrease metabolic substrate supply to the host. This can be overcome by co-infusion of insulin

[northendninja]

thanks einstein, u cleared up this "debate" quite nicely, like frank the tank in old school during the debate scene

I really didnt hold any stock in the t-mag article, but i was chatting with one of my sources about using IGF on my next cycle, and he shot me down, pointing me to this article. Also, most of the references he had listed are quite dated, with no real recent finding (actually no substantial findings at all) to back up his pathetically weak argument that IGF-1 R3 is the worst BB drug ever.

[flexshack]

i cant wait to do it this summer!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! !!!!!!!!!!!!!!!!!!!!!!!!!

i can't wait for the summer. too long. forget the summer, i'm doing it in a few weeks.

[Ozzy]

I just went to Western Union lastnite , I ordered 3mg

[northendninja]

running all 3ml in one cycle?

[Ozzy]

running all 3ml in one cycle?

No way ! I just saw this post now so................I was on for 1 month and then took a month off and now back on it.

[Jacked As Hell]

How did you like it Ozzy?

[chicamahomico]

Excellent debate. TMag usually does cite sources in their articles so I dunno why they wouldn't on this one. Einstein what do you think about the article's claims that IGF-1 is nowhere near as effective as AS for muscle gain?

[jbigdog69]

I read the study...however...it is based on igf-1 and not lr3 igf-1. Big difference Bro's.

[JohnnyB]

I read the study...however...it is based on igf-1 and not lr3 igf-1. Big difference Bro's.

Good point Bro, that why I like calling it LR3 instead of IGF-1 people get info confused. LR3 is an analog of IGF-1 not IGF-1, so the info on hIGF-1 doesn't apply to LR3.

JohnnyB

[JohnnyB]

No way ! I just saw this post now so................I was on for 1 month and then took a month off and now back on it.

Bro I was still see results at 5 weeks I would of kept going but didn't have any LR3 left.

JohnnyB

[einstein1905]

Excellent debate. TMag usually does cite sources in their articles so I dunno why they wouldn't on this one. Einstein what do you think about the article's claims that IGF-1 is nowhere near as effective as AS for muscle gain?

LR3 itself doesn't provide much mass gain, but it does increase protein synthesis of contractile fibers.....it increases strength and hardens you up. However, and most importantly IMO, it provides more potential for mass increases. It does so by increasing cell count numbers of muscle fibers....the higher the cell count, the more androgen receptors....the more androgen receptors, the more potential for greater effects from AAS. It's ability to drop bf is another great perk.

[Russ616]

First off, whoever wrote that must have been on the chapter on apoptosis in their undergrad molecular biology class at the time it was written. I see no purpose to preface an article with the rudimentary mechanisms of the development of cancers and then go on to merely speculate (without referencing any literature) how IGF-1 may fit into this picture. They speculate that IGF-1 (but in particular, LR3) may play a role as catalyst in cancers.....yes....we assume so too. It may exacerbate an existing cancer....that is a potential risk. LR3 is simply a more potent version of physiological IGF-1, so its effects are going to be dose-dependent.....adjust for the appropriate dose, and IGF-1 will have similar effects to LR3. The use of AAS (test) has been shown to increase IGF-1 levels substantially, so those that have been using AAS for years, even decades, have been bathing in this cancer-prone environment for years on end......do you see any significant increase in the incidence of cancers among BBers? The same can be said for GH, which has been around for a while (much longer than LR3).
They allude to a few in vitro assays that potentially have some correlational relevance to the real world (however, they neglect to cite them) but lack an real world evidence of their claims.....I'd tip my hat to them if they even had a rodent model experiment showing increased risk of cancers in response to elevated IGF-1 levels (let alone LR3). It's a pretty bold assertion calling IGF-1 the worst BB supplement without any real evidence to support that claim.

As for the lack of aesthetic effects, you need not look any further than some recent threads where users raved about our experiences with LR3.


You can theorize until you're blue in the face, but if it doesn't translate to the real world, it's all just speculation.

Very nicely put. My question is why do people even use other boards... AR

[flexshack]

LR3 itself doesn't provide much mass gain, but it does increase protein synthesis of contractile fibers.....it increases strength and hardens you up. However, and most importantly IMO, it provides more potential for mass increases. It does so by increasing cell count numbers of muscle fibers....the higher the cell count, the more androgen receptors....the more androgen receptors, the more potential for greater effects from AAS. It's ability to drop bf is another great perk.

well put einstein, but i have one question. do you think it has a finite capacity to increase the potential for mass increases? besides muscle cell mitosis, isn't the only other way for proliferation through the recruitment of satelitte cells? if so, wouldn't there be a finite number of satelittle cells to recruit?

[einstein1905]

Yes, there was a study that overexpressed IGF-1 in rat muscle, and the growth was great for a long period of time, but it eventually tapered and plateaued. They concluded that it was due to lessened supply of satellite cells. I believe satellite cells are mitotic, but the rate of recruitment was faster than the rate of mitosis in their case. Cycling IGF-1 may not pose this problem

[flexshack]

Yes, there was a study that overexpressed IGF-1 in rat muscle, and the growth was great for a long period of time, but it eventually tapered and plateaued. They concluded that it was due to lessened supply of satellite cells. I believe satellite cells are mitotic, but the rate of recruitment was faster than the rate of mitosis in their case. Cycling IGF-1 may not pose this problem

sorry i took a while to reply.
anyway, why would cycling not pose this problem? do satelitte cells go through mitosis even with normal physiological levels of igf-1 (off cycle)? this would be the only reason i could think of that would explain why no problem would occur with cycling. however, if mitosis of satelitte cells only occurred with supraphysiological levels of igf, yet the rate was still slower than recruitment, growth would again retard.

[einstein1905]

sorry i took a while to reply.
anyway, why would cycling not pose this problem? do satelitte cells go through mitosis even with normal physiological levels of igf-1 (off cycle)? this would be the only reason i could think of that would explain why no problem would occur with cycling. however, if mitosis of satelitte cells only occurred with supraphysiological levels of igf, yet the rate was still slower than recruitment, growth would again retard.

Mitosis of satellite cells is independent of IGF-1. So, the rate of satellite cell mitosis was not sufficient to maintain an adequate supply of satellite cells for IGF-1 recruitment.

[flexshack]

Mitosis of satellite cells is independent of IGF-1. So, the rate of satellite cell mitosis was not sufficient to maintain an adequate supply of satellite cells for IGF-1 recruitment.

oh, but if all of the satellite cells are recruited from a cycle of igf-1, wouldn't that leave zero cells for mitosis?

i am guessing that recruitment isn't quite that fast and that mitosis isn't quite that slow. if this is so and all of the satellite cells cannot be recruited even with an igf-1 cycle and mitosis occurs during the off cycle period, you're saying that the satellite cells over enough time will restock or replenish (through mitosis) a large enough supply for recruitment once again?

[einstein1905]

oh, but if all of the satellite cells are recruited from a cycle of igf-1, wouldn't that leave zero cells for mitosis?

i am guessing that recruitment isn't quite that fast and that mitosis isn't quite that slow. if this is so and all of the satellite cells cannot be recruited even with an igf-1 cycle and mitosis occurs during the off cycle period, you're saying that the satellite cells over enough time will restock or replenish (through mitosis) a large enough supply for recruitment once again?

That's the theory. The recruitment of satellite cells isn't 100% efficient. There will never be zero left. It's just that as the supply wanes, the statistical probability of IGF-1 binding receptors on satellite cells, which are in low supply, becomes far less.