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IGF-1 & CANCER/TUMOURS

celtic-devil

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Hi guys,

I was wondering what you guys thought of the link between IGF-1 and the activation of cancerous cell growth/tumours and the proliferation of cancerous cells/tumours.

It doesn’t seem to be something that has really been discussed on this forum (or many other forums for that matter). I believe Cy Wilson (T-nation) wrote about it some time back saying that IGF-1 (or any form of GH/growth factor therapy) can activate cancerous cells in your body which would not otherwise have been activated and/or cause incredibly fast growth of these cancerous cells.

Although I have not researched this in depth I have looked at several other studies/sources that support this. Apparently it’s pretty accepted in the medical field that higher IGF-1 levels can lead to increased activation of cancerous cells and or/extremely fast tumour growth.

Basically from the way I understand it, you can go through life with a cancerous/damaged cell in your body (or many such cells). However, such cells may never be “activated” and begin to divide/grow. IGF-1 can potentially “activate” these cells and also lead to unbelievably fast growth of such cells. Scary shit!!

So, what do you guys think of these risks? They are, most definitely, documented and real. IGF-1 has been linked (significantly) to many types of cancer. Just google IGF-1 and cancer and dozens of studies/medical papers will come up explaining the links between IGF-1 and many types of cancer. Personally, I am a little nervous about taking IGF-1 since both my grandmother (breastcancer) and my cousin (leg tumour) had cancer, so I have some history. ALthough many take IGF-1 and have no problems I believe these risks (especially risks of serious cancer) warrant discussion.

My second thoughts would be, that this would seem to be a systemic effect. Which means that if we just take rhIGF-1 for hyperplasia purposes (as per Grunt76’s protocol) as opposed to IGF-Lr3, we can avoid theses systemic effects of IGF-1 Lr3 since rhIGF-1 has such a short half life that it will not go systemic. Thus, we can avoid the cancer risks as the rhIGF-1 would only ever be acting on the exact muscle injected and will not survive long enough to be able to go systemic and travel to the damaged/potentially cancerous cells in your body.

Anyone care to add their thoughts on this? (anyone any experience with rhIGF-1 also?)

CD
 
Good topic, one that I believe should be discussed more. I am not a dr or smart enough to even comment on these things though.
 
If I was a longtime smoker, I would def not be using igf.
 
A very interesting topic!
I do know that it is documented that GH of which IGF is a derivative leads to cancers growing quicker, therefore i'm sure as you say, IGF will do the same. Whether it can actually activate cancerous activity i'm not sure of.
However, did you know that it is also documented that those who eat less are more likely to live longer. I am not talking skinny people compared to fat people. I mean of those who are within a healthy weight range, those who eat less will live longer.
Obviously you have to eat to grow! And if your a bodybuilder you want to grow... right!
So, how much you eat, how many steroids you consume, IGF consumption (amount used and duration) as you mention will all affect how long you live (along with one million other factors).
As has been said before on this board 'if you wanna play, you you gotta pay'
(i.e. these are the risks you take in order to gain benefits)
But why take these risks to an extreme if you are not a professional bodybuilder/ athlete?
 
I believe they are very possible risks especially, if you have a family history of cancer. Be on the safe side and stick with the science and published data for now.
 
I don't think it a huge issue unless you stay on large doses for long long peroids of time all the time. Think about it. Out of all the guys on the boards,pro's,etc... how many cases have been reported from IGF use? Sure there have been a few studies, but there has not been that many subjects who have been effected.
 
I don't think it a huge issue unless you stay on large doses for long long peroids of time all the time. Think about it. Out of all the guys on the boards,pro's,etc... how many cases have been reported from IGF use? Sure there have been a few studies, but there has not been that many subjects who have been effected.


Well, we will see. Time will tell in the years to come with all the igf-1 use etc. I am sure you will not have people coming forth to report they have cancer and used AAS, IGF-1, GH ETC.


Lancet, Volume 363, Issue 9418, Pages 1346-1353

Insulin-likThe e growth factor (IGF)-I, IGF binding protein-3, and cancer risk: systematic review and meta-regression analysis

DrAndrew G Renehan PhDa, , , Marcel Zwahlen PhDc, ProfChristoph Minder PhDc, Sarah T O'Dwyer MDa, ProfStephen M Shalet MDb and ProfMatthias Egger MDc, d

aDepartment of Surgery, Christie Hospital NHS Trust, Manchester, UK
bDepartment of Endocrinology, Christie Hospital NHS Trust, Manchester, UK
cDepartment of Social and Preventive Medicine, University of Berne, Switzerland
dDepartment of Social Medicine, University of Bristol, UK


Available online 23 April 2004.

Refers to: The growth hormone and insulin-like growth factor I axis, and cancer, The Lancet, Volume 363, Issue 9418, 24 April 2004, Pages 1336-1337
Alicja Wolka,
Abstract | Full Text + Links | PDF (55 K)

Referred to by: The growth hormone and insulin-like growth factor I axis, and cancer, The Lancet, Volume 363, Issue 9418, 24 April 2004, Pages 1336-1337
Alicja Wolka,
Abstract | Full Text + Links | PDF (55 K)

Summary
Background
Insulin-like growth factor (IGF)-I and its main binding protein, IGFBP-3, modulate cell growth and survival, and are thought to be important in tumour development. Circulating concentrations of IGF-I might be associated with an increased risk of cancer, whereas IGFBP-3 concentrations could be associated with a decreased cancer risk.

Methods
We did a systematic review and meta-regression analysis of case-control studies, including studies nested in cohorts, of the association between concentrations of IGF-I and IGFBP-3 and prostate, colorectal, premenopausal and postmenopausal breast, and lung cancer. Study-specific dose-response slopes were obtained by relating the natural log of odds ratios for different exposure levels to blood concentrations normalised to a percentile scale.

Findings
We identified 21 eligible studies (26 datasets), which inHigh concentrations of IGF-I were associated with an increased risk of prostate cancer (odds ratio comparing 75th with 25th percentile 1·49, 95% CI 1·14–1·95) and premenopausal breast cancer (1·65, 1·26–2·08) and high concentrations of IGFBP-3 were associated with increased risk of pre-menopausal breast cancer (1·51, 1·01–2·27). cluded 3609 cases and 7137 controls. Associations were larger in assessments of plasma samples than in serum samples, and in standard case-control studies compared with nested studies.

Interpretation
Circulating concentrations of IGF-I and IGFBP-3 are associated with an increased risk of common cancers, but associations are modest and vary between sites. Although laboratory methods need to be standardised, these epidemiological observations could have major implications for assessment of risk and prevention of cancer.



Anyways here are a few more studies. There are many if you do a basic internet search.

**broken link removed**

**broken link removed**

http://www.medscape.com/viewarticle/522728_6

**broken link removed**

**broken link removed**
 
Last edited:
BTW my posts all pertain to Long R3 unless specifically noted hIGF-1. Let me ring Gavin about these questions.

I have done extensive research on IGF-1, but prior to that I have done extensive research on rejuvenation, which, as made obvious in the more scientific parts of the post above, touches closely at the cellular level to how cancer works or does not work.

What is cancer?
Cancer originates in a mutation of DNA, which makes the cell crazy about replicating itself. Moreover, at the same time that it is made cancerous, a cell expresses (makes an releases) IGF-1 in large quantities. This IGF-1 likely, as pointed at in the article above, makes the original cell and its offspring "forget" that it should not replicate more than a given number of times. Thus it replicates again and again at extremely fast rates, and at the same time give up its normal job, concentrating all the available resources to its growth.

IGF-1 plays an important role in cancer!
Yes, cancerous cells depend on the presence of massive amounts of IGF-1 to protect their telomeres and keep reproducing. And as such, cancer cells are saturated with their own autocrine IGF-1. The evidence points to exogenous IGF-1 being insignificant at the tumor and cell level because the cell itself already expresses large amounts of it. So if you have cancer and take IGF-1, most likely that will not make any difference.

Can IGF-1 CAUSE cancer?
For cancer to happen, DNA must mutate. How do mutations occur? Virii are most likely the main culprit of cancers. For a long time oxidative stress was believed to be the #1 cause, but now more evidence points to virii being the #1 and oxidative stress as being the #2, the two being closely intermingled since oxidative stress impacts the immune system quite effectively, making viral infection more likely.

IGF-1 does not mutate DNA. As a matter of fact, most evidence points to IGF-1 PREVENTING DNA mutations. The telomeres are but one part of the DNA, and IGF-1 helps maintain the status quo of the whole double helix. So while some people are quick to point out that IGF-1 prevents telomere breakdown, it also forgets to point out that it also keeps the rest of the DNA unchanged. Which, in the case of cancer, is a terrible thing, but in the case of a healthy cell, it is a GOOD thing.

But IGF-1 keeps cells living longer than they should!
True, IGF-1 treated cells live longer and can divide more times than the same cell that is untreated. This, in longevity enhancement, is a bit of a holy grail: if you keep your cells living longer, you as an organism, will be younger for longer. It remains true that when exposed to oxidative stress and viral infection, IGF-1 treated cells have a greater likelihood of becoming cancerous, just as you have more chance of getting cancer if you live to 90 than if you live to 50.

What are we to do?
Take your antioxidants! Grapeseed extract, on top of being a truly great antioxidant, has a documented, direct and selective apoptotic effect on malignant cells. Alpha lipoic acid, especially the r- variety, is a universal antioxidant, another holy grail of longevity: it can go inside of all organs, all cells, all organelles, and exert its potent antioxidant properties, protecting your most precious property of all: your DNA sequence. Don't smoke! Drop the junk food! Stop adding synthetic chemicals to your food! Don't eat GMO's! All of these things have a huge direct impact on the probability of someone getting cancer, IGF-1 or not.

Well the fact that all cancerous cells produce vast amounts of IGF-1 for their own use is a heavily documented medical fact, WELL BEYOND any serious argumentation to the contrary. It is unequivocally so. That being absolutely established, the question remains if adding any MORE IGF-1 to these cells will change something. Well people who don't use IGF-1 still DIE from cancer most of the time, so I'm hard pressed to imagine that adding IGF-1 will do something worse... :blink:

There remains a question at the fringe where you have ONE cancerous cell - which does generate plentiful IGF-1 on its own - and the likelihood of its being killed off by the immune system OR live, and the impact of exogenous IGF-1 on that probability. This is unknown to me, although there may well be some research on the topic. I shall seek to find out more.

Technically we all have cancer as cancerous cells are a common occurrence in all living organisms and there are some very well documented cases of spontaneous tumor growth reversal. And there is no more reason for women to avoid IGF-1 than there is for men. If you are at risk of developing cancer, I guess IGF-1 isn't for you, male or female. Just to be on the safe side.

Here is something about grape seed extract and cancer, both prostate and breast:

http://clincancerres.aacrjournals.org/cgi/...full/12/20/6194

http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15039593
http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=14696100
http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12419835
http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=16731759
http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=10914742
 
Great post grunt......very much appreciated. Interesting info.

I'll dig up the old cy wilson article and post it here if I can.

IGF-1 may not be for me...but if I wer to use it I would certainly not use it systemically and would stick with Grunt's protocol for solely hyperplasia. I have to admit, I am tempterd and curious about IGF-1.

Better yet, I may try to source some rhIGF as opposed to IGF-1Lr3 to completely avoid the systemic efects and avoid any cancer risk.

It doesn't seem that anyone has any experience with rhIGF-1 (at least not that they have posted about) ANyone know where to source any as none of the research companies seem to carry it?

CD
 
I was seen by an Endocrinologist for headaches and they found a 3mm pituitary tumor on my anterior pituitary lobe...So in theory,could cycling IGF make this tumor grow,as i was hoping to cycle it soon???
 
I presume you'r not actually serious?? Thats a joke right?

I know we all take risks but cycling IGF when you already have a tumour....Geez man, you may aswell shoot yourself in the head.
 
heres a study I found

Cancer and insulin-like growth factor-I (IGF-1 )
Editorial / British Medical Journal BMJ 2000;321:847-848 7oct00
A potential mechanism linking the environment with cancer risk .

Insulin-like growth factor-I acts as an important mediator between growth hormone and growth throughout fetal and childhood development. Its effects and those of the other insulin-like growth factors are modulated by at least six different binding proteins. The role of insulin-like growth factor-I in promoting cancer has been investigated for many years, but recently the quality and quantity of evidence has increased.1 In particular, a number of prospective studies using stored blood collected up to 14 years before the onset of disease have shown associations between insulin-like growth factor-I and prostate cancer, premenopausal breast cancer, and colon cancer.2-4

The risk of cancer is higher among people with raised concentrations of insulin-like growth factor-I, and it is lower among those with high concentrations of insulin-like growth factor binding protein-3 (the main binding protein). The associations are similar when people whose blood samples were taken soon before diagnosis are excluded from analyses, suggesting that the observed relations are not due to the release of the growth factor by preclinical cancers.2-4

The effects are sizeable and stronger than the effects seen in relation to most previously reported risk factors.1 Weaker evidence from case-control studies suggests that the ratio of insulin-like growth factor-I to insulin-like growth factor binding protein-3 may also be related to the risk of childhood leukaemia and lung cancer. 5 6

The increasing direct epidemiological evidence that relates insulin-like growth factor-I to the risk of cancer is consistent with more circumstantial evidence. Acromegaly, in which high concentrations of growth hormone stimulate production of high concentrations of insulin-like growth factor-I, has been associated with an increased risk of colorectal cancer and breast cancer in some studies and less consistently with prostate, thyroid, and haematological malignancies.7

In many studies anthropometric markers of the activity of insulin-like growth factor-I, such as height and leg length, are associated with cancer incidence, particularly with the cancers for which risk increases with rising concentrations of insulin-like growth factor-I.8 While adult height is not strongly associated with concentrations of insulin-like growth factor-I in cross sectional studies, it may be a marker for this growth factor during childhood growth,9 and this may be the period during which it acts to increase the risk of cancer occurring in later life.3

Additionally, animal studies have shown that high overall intake of energy in early postnatal life is associated with an increased cancer risk, and this association has recently been found in humans.10 In animals, calorie restriction reduces the risk of cancer primarily by reducing the circulating concentrations of insulin-like growth factor-I.11

Support for the link between cancer and this growth factor comes from an understanding of the potential mechanisms. Concentrations of insulin-like growth factor-I could be a surrogate for the activity of sex steroid hormones, which in turn influence the risk of cancer.

However, associations between insulin-like growth factor-I and cancers dependent on sex hormones are stronger than those between directly measured concentrations of sex hormones and these cancers. Insulin-like growth factor-I may increase cell turnover and the susceptibility of cells to malignant transformation both directly and by modulating the effects of sex steroids. The fact that the risk associated with increased concentrations of insulin-like growth factor-I is greater in people whose DNA is more susceptible to damage induced by mutagens supports this suggestion.6

Alternatively, insulin-like growth factor-I might increase the risk of cancer through its anti-apoptotic activity.1 In this case it prevents the programmed death of cells that have been transformed thus interrupting an important process which retards the development of cancer. Experiments using animal and cell cultures have shown that the anti-apoptotic activity of insulin-like growth factor-I is counterbalanced by the activity of insulin-like growth factor binding protein-3, which may have a direct and independent stimulatory action on apoptosis.

Given the increasing evidence of the risk of cancer, caution should be exercised in the exogenous use of either insulin-like growth factor-I or substances that increase concentrations of it. Despite supposedly being restricted to use only in licensed applications, growth hormone is easily available as an anti-ageing treatment and is surprisingly widely used by athletes and body builders, who also use insulin-like growth factor-I. Those who use these products are unlikely to be aware of their potentially harmful effects.

The final accounting on the balance sheet of growth hormone, insulin-like growth factor-I, and chronic disease is uncertain. The increasing evidence of a risk of cancer may be counterbalanced by a protective effect on the risk of cardiovascular disease. Growth hormone deficiency is associated with an adverse cardiovascular risk profile and increased risk of mortality from cardiovascular disease.12 Low concentrations of insulin-like growth factor-I are also associated with cardiovascular morbidity in the elderly.13

Furthermore, the same studies that have shown a positive association between height and cancer risk suggest that greater height is associated with decreases in cardiovascular and all cause mortality.14

The predictive value of insulin-like growth factor-I may be useful in screening for cancer. For example, the ratio of insulin-like growth factor-I to prostate specific antigen may be a better predictor of the development of prostate cancer than the antigen alone.15 Growth hormone antagonists are being investigated as treatments for some cancers and chemotherapeutic agents are being developed to block the activity of insulin-like growth factor-I or to promote the activity of insulin-like growth factor binding protein-3; these agents may offer additional ways of stimulating apoptosis in malignantly transformed cells.

Lastly, better knowledge of the factors that influence overall concentrations of insulin-like growth factor-I may help in devising strategies to prevent cancer at a population level.

Much recent attention has focused on the human genome project and its potential for unravelling the causes of cancer. The genes that have been identified as causing cancer so far account for only a small proportion of major cancers. The rapid and sizeable changes in the incidence of cancer that have been seen during times of economic development coupled with the findings from twin studies - which compare the concordance of cancer risk in identical and non-identical twins to determine the relative influence of genetic and environmental factors - both point to the importance of non-genomic factors.16

The new epidemiological findings about insulin-like growth factor-I provide one potential mechanism through which an array of previously identified environmental risk factors may act.

George Davey Smith, professor, clinical epidemiology.
David Gunnell, senior lecturer, epidemiology and public health.

Department of Social Medicine, University of Bristol, Bristol BS8 2PR

Jeff Holly, professor, clinical science.

Department of Surgery, University of Bristol


------------------------------------
------------------------------------

1. Holly JMP, Gunnell DJ, Davey Smith G. Growth hormone, IGF-I and cancer. Less intervention to avoid cancer? More intervention to prevent cancer? J Endocrinol 1999; 162: 321-330[Medline].

2. Chan JM, Stampfer MJ, Giovannucci E, Gann PH, Ma J, Wilkinson P, et al. Plasma insulin-like growth factor-I and prostate cancer risk: a prospective study. Science 1998; 279: 563-566[Abstract/Full Text].

3. Hankinson SE, Willett WC, Colditz GA, Hunter DJ, Michaud DS, Deroo B, et al. Circulating concentrations of insulin-like growth factor-I and risk of breast cancer. Lancet 1998; 351: 1393-1396[Medline].

4. Ma P, Pollak MN, Giovannucci E, Chan JM, Tao Y, Hennekens CH, et al. Prospective study of colorectal cancer risk in men and plasma levels of insulin-like growth factor (IGF)-I and IGF-binding protein-3. J Natl Cancer Inst 1999; 91: 620-625[Abstract/Full Text].

5. Petridou E, Dessypris N, Spanos E, Mantzoros C, Skalkidou A, Kalmanti M, et al. Insulin-like growth factor-I and binding protein-3 in relation to childhood leukaemia. Int J Cancer 1999; 80: 494-496[Medline].

6. Wu X, Yu H, Amos CI, Hong WK, Spitz MR. Joint effect of insulin-like growth factors and mutagen sensitivity in lung cancer risk. J Natl Cancer Inst 2000; 92: 737-743[Abstract/Full Text].

7. Jenkins P. Cancer in acromegaly. Trends Endocrinology Metab 1998; 9: 360-366.

8. Gunnell D. Height, insulin-like growth factors and cancer risk. Growth Horm IGF Res 2000; 10(suppl A): 39-40S.

9. Juul A, Bang P, Hertel NT, Main K, Dalgaard P, Jorgensen K, et al. Serum insulin-like growth factor-I in 1030 healthy children, adolescents, and adults: relation to age, sex, stage of puberty, testicular size, and body mass index. J Clin Endocrinol Metab 1994; 78: 744-752[Medline].

10. Frankel S, Gunnell DJ, Peters TJ, Maynard M, Davey Smith G. Childhood energy intake and adult mortality from cancer: the Boyd Orr cohort study. BMJ 1998; 316: 499-504[Abstract/Full Text].

11. Dunn SE, Kari FW, French J, Leininger JR, Travlos G, Wilson R, et al. Dietary restriction reduces insulin-like growth factor I levels, which modulated apoptosis, cell proliferation, and tumor progression in p53-defieicnt mice. Cancer Res 1997; 57: 4667-4672[Medline].

12. Sacca L, Cittadine A, Fazio S. Growth hormone and the heart. Endocr Rev 1994; 15: 555-573[Abstract].

13. Janssen JAMJL, Stolk RP, Pols HAP, Grobbe DE, Lamberts SWJ. Serum total IGF-I, free IGF-I and IGFBP-1 levels in an elderly population. Relation to cardiovascular risk factors and disease. Arterioscler Thromb Vasc Biol 1998; 18: 277-282[Abstract/Full Text].

14. Davey Smith G, Hart C, Upton M, Hole D, Gillis C, Watt G, et al. Height and risk of death among men and women: aetiological implications of associations with cardiorespiratory and cancer mortality. J Epidemiol Commun Health 2000; 54: 97-103[Abstract/Full Text].

15. Djavan B, Bursa B, Seitz C, Soeregi G, Remzi M, Basharkhah A, et al. Insulin-like growth factor-I (IGF-I), IGF-I density and IGF/PSA ratio for prostate cancer detection. Urology 1999; 54: 603-606[Medline].

16. Lichtenstein P, Holm NV, Verkasalo PK, Iliadou A, Kaprio J, Koskenvuo M, et al. Environmental and heritable factors in the causation of cancer -- analyses of cohorts of twins from Sweden, Denmark, and Finland. N Engl J Med 2000; 343: 78-85[Medline].
 
Celtic-Devil........Thanks for the read,very informative and opened my eyes alot :D Just a pity that i can't cycle now..Saying that tho,my endo said that about 5% of the British public have pit swellings/tumors and don't even know,as they never show symptoms.
So if a bodybuilder who has an unknown tumor was to administer IGF,would it grow at an accelerated speed in EVERY case? Pituitary tumors are 99.9% proven to be non cancerous too!
 
heres a study I found

I posted that one up a few months ago, but nobody really read it or responded to the post.
 
Last edited:
LOL.....

Looks like you beat me to it dragonfire :) Have you looked into the issue much? I'd love if you could add any info to the thread that you might have...

Simm - like Grunt posted above, we do know that cancer cells produce massive amounts of IGF and that is a major facor in their uncontrollable division. However, they produce this IGF-1 themselves in huge amounts so it is unclear to me at the moment (would have to look into it further) whether exogenous IGF-1 would accelerate cancerous growth even further. Possibly a few of the others could chime in on this...any extra info is appreciated.

One thing is for sure though, if you have a tumour you should not even be THINKING about cycling IGF-1, or any growth factors (GH, MGF etc) for that matter...the risk is honestly not worth it bro. The science would suggest that you should hold off IGF-1. Even in the future when you are recovered from the tumour, I would certainly never run growth factors again as you may have an unfortunate pre-disposition to cancers. Sorry to scare you bro, but it's far better to be safe than sorry and I wouldn't like to see you possibly worsening any condition you have.

Perhaps you could run it by your doc or any specialists you might see as he may have valuable input in the role of exogenous IGF-1 in cancer cell growth. With something as serious as cancer, It may be a good idea to be as honest & candid as possible with your doctor and disclose any past IGF-1 use. (keeping in mind that it may affect your health insurance btw)

In any case, I hope your situation doesn't turn out to be too serious.
 
SUPER DUPER STUDY, THANK YOU!!! I absolutely agree with celtic-devil.

I use IGF-1 regularly. However, I have never smoked cigarettes, I don't drink alcohol, I eat all-organic, and I live a low stress lifestyle. Moreover, in all my family tree including cousins & even further on, there was only ONE case of cancer, my grandfather at 80+, alcoholic and addicted to the spiciest foods. Esophagus cancer. I also religiously take my grape seed extract which has HUGE anti-cancer effects.

I think I am much better off than most smokers even with my IGF-1. YMMV.
 
Celtic-Devil...I really appreciate your help and all the study reports you have posted here! I am totally 100% not even considering IGF use now! Thanks again! ;)
 

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