71sport408
New member
Thought I'd do a little reading on IGF-1 and so I did. Thirty pages later and I'm astounded. Thanks to all that contributed, especially Grunt.
My take on IGF-1
- Thread starter Grunt76
- Start date
datBtrue
Well-known member
IGF-I, IGF-II & Insulin
Although the source material may not be really current I thought the following paragraphs describing similarities between IGF-I, IGF-II & Insulin were interesting.
SOURCE: Hormones, second edition, Anthony W. Norman, Academic Press, 1997
Although the source material may not be really current I thought the following paragraphs describing similarities between IGF-I, IGF-II & Insulin were interesting.
SOURCE: Hormones, second edition, Anthony W. Norman, Academic Press, 1997
The growth-promoting activity of insulin itself is due to its limited ability to bind to IGF-I receptor. To do this, insulin has to be present in high concentrations because the affinity of the IGF-I receptor for insulin is about 1000x less than the affinity of the insulin receptor for insulin. IGF-II can also productively bind to the IGF-I receptor, albeit with much lower affinity. Thus, all three factors are growth-promoting, and IGF-II and insulin become important when IGF-I is low or absent. Presumably, IGFs can cross over to the insulin receptor in the absence of insulin, although this sort of rescue may not be important in insulin-deficient diabetes.
Interestingly, as shown in Figure 5-29, the level of circulating somatomedin (IGFs) increases to a maximum until about 8 years of age when the human adult level is reached. Since growth continues for many years beyond age 8, it is obvious that the amount of circulating somatomedins is not rate-limiting for growth. Thus, some other component of the overall system may limit growth, such as the development of somatomedin receptors or some other factor involved in the utilization of these mitogens. Somatomedins also stimulate sulfation, and this is important to bone growth. - p. 156
Similarities between some groups of ligands indicate that they may have derived from the same or similar ancestors. Examples are insulin, IGF-I, and IGF-II. This group shares homology to the extent that there can be crossover binding to their receptors. For example, both insulin and IGF-II can bind to the IGF-I receptor, although much greater amounts of IGF-II and insulin are needed to activate the receptor. However, it appears that blockage of IGF-I by competition with a similar but inactive peptide, while greatly inhibiting the growth of certain cells in culture, has a much smaller effect on intact animals. Perhaps this is indicative of the growth factors (e.g., insulin or IGF-II) that are present in great enough quantity to overcome the effect of the inhibitor. - p. 487
III. INTERACTION OF IGFs WITH RECEPTORS
Not only do IGFs and insulin have high homologies, but the receptors for IGF-I and insulin are also homologous. Thus, IGF-I receptor binds IGF-I and, at higher levels, insulin, and it also carries binding sites for IGF-II which are apparently different from the sites to which IGF-I binds. The beta-subunits of both receptors contain a tyrosine kinase and ligand binding triggers the activity of the tyrosine kinase, resulting in autophosphorylation on tyrosine residues. Other proteins may be phosphorylated on tyrosine residues by the receptor kinase. IGF-I receptors are present in most tissues: the hormone exerts its effect in concert with other hormones produced in specialized tissues, and the IGF-I receptor is down-regulated after ligand binding in a typical process characteristic of many membrane receptors. IGF-II receptors bind IGF-II nearly exclusively and interact poorly with IGF-I. On the other hand, as has already been pointed out, IGF-II can bind to the IGF-I receptor and this interaction is important in humans, who, in contrast to some rodents, produce IGF-II. The IGF-II receptor is identical to the mannose 6- phosphate receptor and contains separate domains for binding IGF-II and mannose 6-phosphate. Interestingly, the mannose 6-phosphate-binding domain activates the TGF-beta* precursor by removing mannose, and this domain has other activities as well. The interaction of IGF-II with the IGF-II receptor may lead to the uptake of extracellular calcium possibly mediated by a G protein. - p. 499
My NOTE: TGF = Transforming Growth Factor
Interestingly, as shown in Figure 5-29, the level of circulating somatomedin (IGFs) increases to a maximum until about 8 years of age when the human adult level is reached. Since growth continues for many years beyond age 8, it is obvious that the amount of circulating somatomedins is not rate-limiting for growth. Thus, some other component of the overall system may limit growth, such as the development of somatomedin receptors or some other factor involved in the utilization of these mitogens. Somatomedins also stimulate sulfation, and this is important to bone growth. - p. 156
Similarities between some groups of ligands indicate that they may have derived from the same or similar ancestors. Examples are insulin, IGF-I, and IGF-II. This group shares homology to the extent that there can be crossover binding to their receptors. For example, both insulin and IGF-II can bind to the IGF-I receptor, although much greater amounts of IGF-II and insulin are needed to activate the receptor. However, it appears that blockage of IGF-I by competition with a similar but inactive peptide, while greatly inhibiting the growth of certain cells in culture, has a much smaller effect on intact animals. Perhaps this is indicative of the growth factors (e.g., insulin or IGF-II) that are present in great enough quantity to overcome the effect of the inhibitor. - p. 487
III. INTERACTION OF IGFs WITH RECEPTORS
Not only do IGFs and insulin have high homologies, but the receptors for IGF-I and insulin are also homologous. Thus, IGF-I receptor binds IGF-I and, at higher levels, insulin, and it also carries binding sites for IGF-II which are apparently different from the sites to which IGF-I binds. The beta-subunits of both receptors contain a tyrosine kinase and ligand binding triggers the activity of the tyrosine kinase, resulting in autophosphorylation on tyrosine residues. Other proteins may be phosphorylated on tyrosine residues by the receptor kinase. IGF-I receptors are present in most tissues: the hormone exerts its effect in concert with other hormones produced in specialized tissues, and the IGF-I receptor is down-regulated after ligand binding in a typical process characteristic of many membrane receptors. IGF-II receptors bind IGF-II nearly exclusively and interact poorly with IGF-I. On the other hand, as has already been pointed out, IGF-II can bind to the IGF-I receptor and this interaction is important in humans, who, in contrast to some rodents, produce IGF-II. The IGF-II receptor is identical to the mannose 6- phosphate receptor and contains separate domains for binding IGF-II and mannose 6-phosphate. Interestingly, the mannose 6-phosphate-binding domain activates the TGF-beta* precursor by removing mannose, and this domain has other activities as well. The interaction of IGF-II with the IGF-II receptor may lead to the uptake of extracellular calcium possibly mediated by a G protein. - p. 499
My NOTE: TGF = Transforming Growth Factor
Grunt76
Well-known member
About the part in red:
There is no evidence whatsoever that warrants saying this, quite the contrary actually. Cancerous cells are incredible IGF-1 factories. They make great amounts of the stuff, which they use themselves. They self-saturate with their IGF-1, at which point it makes no difference whatsoever if exogenous IGF-1 is added.
Bobaslaw
Member
Very interesting Grunt. However, can you shed more light on why then is GH therapy not recommended for patients with cancer? All the medical info on this topic leads to the assumption that you do not want to increase IGF-1 levels in the body mediated by exogenous GH. From this I surmize you would not want to introduce exogenous IGF-1 either.
Basically, say you got cancer (just hypothetical), would you be totally comfortable with your statement and continue with exogenous IGF-1, just because of the info you presented that states cancerous cells are already supplying themselves adequet IGF-1 regardless of the additional levels added via an IGF-1 protocol?
Very interested and curious about this, hope you can shed more light on your feelings regarding this.
EDIT: Added some info:
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Sergio Rossi
New member
Bob / Grunt
I´ve seen divergent statements in the several articles I read out there, but mostly and mostly of them states the same of that articles put by Bob, specially like this one:
“…BRISTOL, UNITED KINGDOM. Several studies have shown powerful associations between blood levels of insulin-like growth factor-I (IGF-1) and the risk of colon cancer, prostate câncer…”
In addition to this, some scientists mention just “growth factors” in their studies of cancer, GH and IGF, what leads me to think of MGF. I started to research if MGF, as a growth factor, can also be involved in (somehow) cancer/tumor risks like IGF-1. Personally, I think so.
As far as me, I did not think of it before but in the past I had some lipoma, which is a kind of tumour of fatty tissue. Its better to be conservative and not take the risk…unfortunally IGF-1 is not for me. Well, only MGF is left as a possible option for while.
Bob, thanks for your previous reply…when I touched the topic of permanent gains in my post…yes, I was talking about hyperplasia. Thanks.
Thanks for clarifications
I´ve seen divergent statements in the several articles I read out there, but mostly and mostly of them states the same of that articles put by Bob, specially like this one:
“…BRISTOL, UNITED KINGDOM. Several studies have shown powerful associations between blood levels of insulin-like growth factor-I (IGF-1) and the risk of colon cancer, prostate câncer…”
In addition to this, some scientists mention just “growth factors” in their studies of cancer, GH and IGF, what leads me to think of MGF. I started to research if MGF, as a growth factor, can also be involved in (somehow) cancer/tumor risks like IGF-1. Personally, I think so.
As far as me, I did not think of it before but in the past I had some lipoma, which is a kind of tumour of fatty tissue. Its better to be conservative and not take the risk…unfortunally IGF-1 is not for me. Well, only MGF is left as a possible option for while.
Bob, thanks for your previous reply…when I touched the topic of permanent gains in my post…yes, I was talking about hyperplasia. Thanks.
Thanks for clarifications
datBtrue
Well-known member
From the Journal of Anti-Aging Medicine article you posted Bob...
The point is cancer is opportunistic ...some cancer will use any and all IGF-1 available to grow ...if there is not a lot of circulating IGF-1 it will increase the expression of receptors ...some cancer will soak it all up no matter how much is available.
Perhaps if you are diagnosed w/ cancer a good approach might be to contact a legitimate Research site and buy the binding proteins which you will then use to reduce the amount of circulating IGF-1 your body is producing (as a way to counter cancer's opening gambit).
High levels of IGF-1 and other growth factors seem to be a problem only once cancer arises. At other times high levels in the normal range of many hormones contribute to the overall health and well-being of the individual which should to some degree help prevent cancer in the first place.
When I see the medical "establishment" attempt to diminish the use of 1 or 2 ius of exogenically administered growth hormone in aging adults w/ greatly declined levels I stop and consider the source and then I realize that I and a lot of people that frequent this forum understand far more than they do.
But when I see that those same people attempt to tarnish growth hormone replacement by linking it to "in vitro" or artificially constructed protocols for administration to gene-altered mice without examining the fairly large pool of aging humans undergoing hormone replacement and without mentioning those built-in factors inherit in Growth Hormone that would inhibit cancer growth well ....at the very least I don't read their conclusions as conclusive nor do I use them as rational for anything scientific.
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The point is cancer is opportunistic ...some cancer will use any and all IGF-1 available to grow ...if there is not a lot of circulating IGF-1 it will increase the expression of receptors ...some cancer will soak it all up no matter how much is available.
Perhaps if you are diagnosed w/ cancer a good approach might be to contact a legitimate Research site and buy the binding proteins which you will then use to reduce the amount of circulating IGF-1 your body is producing (as a way to counter cancer's opening gambit).
High levels of IGF-1 and other growth factors seem to be a problem only once cancer arises. At other times high levels in the normal range of many hormones contribute to the overall health and well-being of the individual which should to some degree help prevent cancer in the first place.
When I see the medical "establishment" attempt to diminish the use of 1 or 2 ius of exogenically administered growth hormone in aging adults w/ greatly declined levels I stop and consider the source and then I realize that I and a lot of people that frequent this forum understand far more than they do.
But when I see that those same people attempt to tarnish growth hormone replacement by linking it to "in vitro" or artificially constructed protocols for administration to gene-altered mice without examining the fairly large pool of aging humans undergoing hormone replacement and without mentioning those built-in factors inherit in Growth Hormone that would inhibit cancer growth well ....at the very least I don't read their conclusions as conclusive nor do I use them as rational for anything scientific.
pumbertot
Active member
yes I have to agree with this. certainly we treat many different types of cancers at work and its only in specific types of malignant cancers that Somatostatin (Octreotide) is considered to be usefull. When I asked one of our professors the reason for this, he said that only in these types of cancers is growth hormone considered to be in danger of 'feeding' the tumour.
i.e. you need to have highly malignant tumours in the first place to have to worry about HGH or IGF use, and in those instances you are probably f*cked already, to be blunt.
Bobaslaw
Member
Seems that there are a few rationales regarding cancer and IGF-1 (GH mediated or exogenous).
One is that cancers that have a greated expression of IGF-1 receptors will be agonized to a greater degree.
The other is indirect. I will describe it like this (per what I have found in some research):
DNA mutations in cells is a natural occurence. A certain % of all proliferated cell lines produce a certain % of mutated or cancerous cells which are usually dealt with appropriately by the bodys defenses against this. Well, if you increase IGF-1 levels for a long period (as is proposed), then you increase the proliferation rate of cells and thus the number of cell mutations in a given timeframe. This increases the chances that some of these cells may make it and proliferate and not be dealt with accordingly. Obviously other factors would have to coincide with this, so this is not a "sole" reason for cancer mediated by IGF-1.
BTW, this is not my opinion, just what I have read in some of my research.
One is that cancers that have a greated expression of IGF-1 receptors will be agonized to a greater degree.
The other is indirect. I will describe it like this (per what I have found in some research):
DNA mutations in cells is a natural occurence. A certain % of all proliferated cell lines produce a certain % of mutated or cancerous cells which are usually dealt with appropriately by the bodys defenses against this. Well, if you increase IGF-1 levels for a long period (as is proposed), then you increase the proliferation rate of cells and thus the number of cell mutations in a given timeframe. This increases the chances that some of these cells may make it and proliferate and not be dealt with accordingly. Obviously other factors would have to coincide with this, so this is not a "sole" reason for cancer mediated by IGF-1.
BTW, this is not my opinion, just what I have read in some of my research.
Grunt76
Well-known member
This is exactly why I believe injecting IGF-1 3 times a week is a MUCH healthier option than going at it twice a day every day as PA suggests.
pumbertot
Active member
yes a bit like tanning and melanomas. as you increase the mutation rate of skin cells, you increase the chances of skin cancer.
ah well I for one believe the benefits of peptides are worth the increased risk.
datBtrue
Well-known member
Yes maybe ...even more importantly it could possibly interfere w/ apoptosis...I am more concerned about this in the prostate because that is where it seems the most accumulation of cells gone awry or mutations occur and build up over time.
I just read through the patent filing for various types and methods of making an injectable curcumin vehicle, filed by doctors from MD Anderson Cancer Center... it is a very informative filing because as you know curcumin has been shown to induce cancer cell apotosis but has poor bioavailability.
I know Bob. You have a wonderfuly curious mind... I wasn't criticizing you ...I respect you and learn from you.
datBtrue
Well-known member
Yes I am rethinking my 10mcg per day for 3 months protocol as well....well I've just rethought it and I think I have now abandon it.
Grunt76
Well-known member
That is one interesting patent filing. Cool beans! :hammer:
As well grape seed extract has been shown to directly trigger apoptosis of precancerous and cancerous cells but not of healthy cells of the same tissue, both in vitro and in vivo. :woohoo:
datBtrue
Well-known member
The key part of the filing is all the types of delivery systems mostly liposomes which may have unique affinity for different types of target tissue. So you try to create one system to target the prostate ...you go to legitimate research sites and you find the compounds you need to create the liposome vehicle and sort through the nomenclature to find the one w/ just the right ionic charge...
...its a lot of work for a lay-person but I'm going to make it a hobby I think. I'm looking into buying a used commercial lypholizer...I think...if I can get ahold of a manual first before I buy so I can be sure I'll be able to operate it.
Bobaslaw
Member
Likewise DBT! Thank You.
BTW, I did not think at any point that you were criticizing me. I just realized that in some of my posts I tend to make statements that at partly opinion, but I do not make this known. I definitely do not want to spread anything that is not factual, while represented as such
I do appreciate your sentiment greatly
CryingEmo
Well-known member
Bobaslaw is a propreitary AI developed by physicists at Los Alamos. He runs on a customized linux OS running on a beowulf cluster, optimized for researching ways for pale skinny scientists to get buff.
Xodus
Well-known member
Now you are talking! I ran a small Beowolf cluster for awhile at my house, but then 'graduated' to OpenMosix, unfortunately it wasn't for the benefit of getting buff.
longrob
Member
Bob, let me ask you a question. I had a basal cell carcinoma removed from my forearm 3 years ago. Should I therefore not use IGF-1LR3 for fear of growing more?
Bobaslaw
Member
If it were me, personally I would not use any exogenous IGF-1 or GH given the info currently presented, especially if I was predisposed to cancer or had any type of cancer at any point in my life.
I am sure this may possibly be open to different opinions and viewpoints here, and I am very interested to see what others would do if they were in your place. Somehow I feel most would side more with lower risk route.
Curious to see others opinions, Grunt, DatBTrue, Pumbertot, etc... Of course how can I forget CryingEmo.
BTW CE, since using IGF-1 the number of nodes in my cluster have proliferated from 16 to 32. Maybe some Test-E/Deca for maximum hyperthreading at some point
Sergio Rossi
New member
Guys...I know that these posts are about IGF-1, but what´s your opinion on MGF use (regarding the cancer risk we´ve talking about) ? Could I assume a person would be exposed to the same risks of IGF-1, or it works on different pathways?
tks
tks
nephilim666
Well-known member
i would like to throw some imput into this discussion reguarding cancers. a relative of mine is a chemist for organon, and we got into a discussion about how i use growth factors. He said if you have a predisposition to cancer that the use of growth factors will speed it up. if you HAVE cancer certain growth factors will make it much worse. getting a test done before use of gf's will be a pretty wise decision 
another interesting thing he stressed was that high doses are not nessesary. the higher the dose the increased risk of mutant cells. he said many growth factors will cause mutations in cells, not nessesarily being harmful or cancerous, but mutations nontheless.
another interesting thing he stressed was that high doses are not nessesary. the higher the dose the increased risk of mutant cells. he said many growth factors will cause mutations in cells, not nessesarily being harmful or cancerous, but mutations nontheless.
Bobaslaw
Member
please see post#911 at it touches on this and what Grunt thinks about dosing related to this.
Also, IMO GFs such as IGF does not "cause" mutations directly. Mutations occur naturally. Naturally, a certain percentage of proliferated cells in tissues will become damaged or mutated and possibly cancerous. Increasing the cell proliferation rate in various tissues via GH or IGF regimen would mathematically exhibit a higher number of mutated cells in a given time frame, compared to baseline. This can possibly increase the chances some of these cells could become cancerous.
nephilim666
Well-known member
agreed. it doesnt cause cancer directly but it does increase the number of cells that will mutate.
Grunt76
Well-known member
That is the same statement as saying "the longer you live, the more likely you are to have cancer"... Just for perspective.
Bobaslaw
Member
I totally agree. Kinda like saying, the more you fly, the more likely you will be in a plance crash. How dramatic is the impact of this really (the statement NOT the crash)
IMO, not worth the worry...
nephilim666
Well-known member
well yea thats y im not guna stop using these chems. idc if i end up getting cancer in 15 years because by then it will be a readily curable disease. more and more cancers are becoming survivable that years ago would be fatal.
pumbertot
Active member
yes but unfortunately its so true too. if us men live beyond 80,our chances of NOT getting prostate cancer are only 10%.
on to the question about using igf-1 after removal of cancer.
although I wouldnt recommend it to all, I presonally wouldnt change how I do things as Id rather die big and young than die old and small, but then Im a little f*cked up in the head.
nephilim666
Well-known member
agreed why would i wana get old and get small. not for me. being small is probably the worst thing that could happen. then thers dying, but thats 2nd to being small :hammer::woohoo:
Grunt76
Well-known member
Grape seed extract has been shown to be an incredible antidote for gender cancers, such as prostate, testicles, ovaries, breast etc. Why this knowledge is not more common is way beyond me.
pumbertot
Active member
Bobaslaw
Member
drink it or inject it?
Hey Pumber,
A grape suppository could yield better results, you should do a log
Grunt76
Well-known member
Hey Pumber,
A grape suppository could yield better results, you should do a log
Good idea!
Although, Bobaslaw would probably want to see pictures of the administration procedure... :aargh:
stankydanky
New member
for a long term lr3 igf-1 dosing scheme, would 15mcg bilateral in each muscle group (30mcg 3x a week) be a stupid idea? Would i be better off sticking to 30mcg in each muscle group (60mcg 3x a week) when it comes to a pure muscle hypertrophy perspective? Thanks.
Ive read that we dont produce nearly as much as 5mcg so i figure 15mcg bilateral 3x a week would be practical.
Ive read that we dont produce nearly as much as 5mcg so i figure 15mcg bilateral 3x a week would be practical.
pumbertot
Active member
no thats not a stupid idea, your reasoning is sound imo.
pumbertot
Active member
pump is immediate. vascularity after about 3 weeks. fat loss takes a bit longer than both.
papapumpsd
Well-known member
Do you have any feedback regarding muscle gains and fat loss post cycle? I'm talking about 1-3 months down the road....what can one expect?
rippedfreak123
New member
when i took it, i experienced more than anything massive pumps and great fullness which in return made me look larger just not ading all that water and weight
pumbertot
Active member
sure, its been 7 weeks since my last igf shot. gained around
2-3kg in 7 weeks and lost 1-2% bf in conjuction with mgf/pegmgf
rippedfreak123
New member
papapumpsd
Well-known member
So, the 7th week from the LAST injection you gained 2-3kg and lost 1-2% BF? This is on top of your gains while you were "on"?
Mind sharing the total muscle gains and fat losses from Day 1 up til now? This is very interesting!
meat250
New member
how would one incorporate CJC and IGF together? so far im thinkin of runnin 40mcg IGF R3 EOD, and 2mg cjc per week, 1mg/2 per week...is there anythin i need to know about the cjc, like when using mgf and igf, mgf should not be used within 12hrs of igf use..any suggestions?
Thanks,
meat
Thanks,
meat
bdazzler
New member
refrigerate IFG-1
Does anyone know if you refrigerate your IGF-1 after the reconstitution of AA or do you just keep it in a cool dry space?
Does anyone know if you refrigerate your IGF-1 after the reconstitution of AA or do you just keep it in a cool dry space?
pumbertot
Active member
as long as not exposed to heat will be fine.