Cancer & "GH"

[klbsa]

What is the real truth about IGF and cancer? It promotes cellular growth, so the chances of cancer would def go up right?

I REALLY want to give it a try but I am scared that I am going to end up with cancer or something.

Am I being silly? I don't have to worry if Im just running a few months right?

 

[Michael Scally MD]

What is the real truth about IGF and cancer? It promotes cellular growth, so the chances of cancer would def go up right?

I REALLY want to give it a try but I am scared that I am going to end up with cancer or something.

Am I being silly? I don't have to worry if Im just running a few months right?

See: https://thinksteroids.com/community/threads/134286559

 

[Michael Scally MD]

Child CJ, Conroy D, Zimmermann AG, Woodmansee W, Erfurth EM, et al. Incidence of Primary Cancers and Intracranial Tumour Recurrences in Growth Hormone-Treated and Untreated Adult Hypopituitary Patients: Analyses from HypoCCS. European Journal of Endocrinology. http://www.eje-online.org/content/early/2015/03/25/EJE-14-1123.abstract

Objective: Speculation remains that growth hormone (GH) treatment is associated with increased neoplasia risk. Studies in GH-treated childhood cancer survivors suggested higher rates of second neoplasms, while cancer risk data for GH-treated and untreated hypopituitary adults have been variable. We present primary cancer risk data from the Hypopituitary Control and Complications Study (HypoCCS) with a focus on specific cancers, and assessment of recurrence rates for pituitary adenoma (PA) and craniopharyngioma (CP).

Design: Incident neoplasms during HypoCCS were evaluated in 8418 GH-treated/1268 untreated patients for primary malignancies, 3668 GH-treated/720 untreated patients with PA history, and 956 GH-treated/102 untreated patients with CP history.

Methods: Using population cancer rates, standardised incidence ratios (SIRs) were calculated for all primary cancers, breast, prostate, and colorectal cancers. Neoplasm rates in GH-treated vs untreated patients were analysed after propensity score adjustment of baseline treatment group imbalances.

Results: During mean follow-up of 4.8 years, 225 primary cancers were identified in GH-treated patients, with SIR of 0.82 (95% confidence interval [CI] 0.71-0.93). SIRs (95% CI) for GH-treated patients were 0.59 (0.36-0.90) for breast, 0.80 (0.57-1.10) for prostate, and 0.62 (0.38-0.96) for colorectal cancers. Cancer risk was not statistically different between GH-treated and untreated patients (relative risk [RR]=1.00 ( 95% CI: 0.70-1.41) p=0.98). Adjusted RR for recurrence was 0.91 (0.68-1.22) p=0.53 for PA and 1.32 (0.53-3.31) p=0.55 for CP.

Conclusions: There was no increased risk for all sites, breast, prostate, or colorectal primary cancers in GH-treated patients during HypoCCS. GH treatment did not increase risk of PA and CP recurrences.

 

[hotdog23]

Dose and duration will play a role. If your IGF is double your reference range and stayed there I'd imagine it would b dangerous territory. Ex. Bodybuilding doses

 

[alphastrength50]

only if you were prone to cancer in the first place. ie. cancerous cells will accelerate growth from hugher igf if you have cancerous cells to begin with

 

[Michael Scally MD]

Raman S, Grimberg A, Waguespack SG, Miller BS, Sklar CA, et al. Risk of Neoplasia in Pediatric Patients Receiving Growth Hormone Therapy - A Report from the Pediatric Endocrine Society Drug and Therapeutics Committee. The Journal of Clinical Endocrinology & Metabolism. http://press.endocrine.org/doi/abs/10.1210/jc.2015-1002

Context: GH and IGF-I have been shown to affect tumor growth in vitro and in some animal models. This report summarizes the available evidence on whether GH therapy in childhood is associated with an increased risk of neoplasia during or after treatment is completed.

Evidence Acquisition: PubMed search conducted through February 2014retrieved original articles written in English addressing GH therapy and neoplasia risk. Subsequent searches were done to include additional relevant publications.

Evidence Synthesis: In children without prior cancer or known risk factors for developing cancer, the clinical evidence does notaffirm an association between GH therapy during childhood and neoplasia. GH therapy has not been reported to increase risk for neoplasia in this population, although most of these data are derived from post-marketing surveillance studies lacking rigorous controls. In patients who are at higher risk for developing cancer, current evidence is insufficient to conclude whether or not GH further increases cancer risk. GH treatment of pediatric cancer survivors does not appear to increase the risk of recurrence, but may increase their risk for subsequent primary neoplasms.

Conclusions: In children without known risk factors for malignancy, GH therapy can be safely administered without concerns about an increased risk for neoplasia. GH use in children with medical diagnoses predisposing them to development of malignancies should be critically analyzed on an individual basis, and if chosen, appropriate surveillance for malignancies should be undertaken. GH can be used to treat GH deficient childhood cancer survivors who are in remission with the understanding that GH therapy may increase their risk for second neoplasms.

 

[A-a-Ron]

What is the real truth about IGF and cancer? It promotes cellular growth, so the chances of cancer would def go up right?

I REALLY want to give it a try but I am scared that I am going to end up with cancer or something.

Am I being silly? I don't have to worry if Im just running a few months right?

My understanding from one of my friends that has a rare form of lymphoma (luckily it was discover on a total fluke and doctors said it would probably be 30 years before he even had to worry) is that everyone has cancer cells in them...it is whether they are active or not that matters. So if you have cancer in you that is active, you could accelerate the growth. If not, you are ok. That's just my understanding from what I've read.

 

[Michael Scally MD]

Berglund A, Gravholt CH, Olsen MS, Christiansen JS, Stochholm K. Growth hormone replacement does not increase mortality in patients with, childhood-onset growth hormone deficiency. Clinical Endocrinology. http://onlinelibrary.wiley.com/doi/10.1111/cen.12848/abstract

Context Long-term safety of growth hormone (GH) treatment is an area of much debate. Studies including children treated with GH not only due to GHD, but also due to non-GHD causes like idiopathic short stature or like short stature in children born small for gestational age, have suggested that GH treatment is associated with increased mortality or stroke.

Objective To study the impact of GH replacement on overall and cause-specific mortality in childhood-onset GHD (CO GHD) patients.

Design A nationwide population-based registry study on CO GHD patients and general population controls matched on age and gender. Mortality hazard ratios (HR) were computed comparing patients and controls, and comparing GH-replaced patients and non GH-replaced patients, using Cox Regression. Comparing GH- and non GH-replaced patients HRs were adjusted for birth year, year of diagnosis, gender, irradiation, ACTH insufficiency, and primary disease.

Patients and Controls 494 CO GHD patients each matched with 100 general population controls were included.

Results Mortality was substantially increased comparing CO GHD patients and general population controls, HR = 7.51 (95% CI=6.06-9.31). Comparing GH-replaced patients with non GH-replaced patients mortality was significantly decreased in total (HR=0.27, CI=0.17-0.43), and due to malignancy (HR=0.14, CI=0.07-0.28) in GH-replaced patients. Adjusting for relevant confounders this decrease remained significant both in total (HR=0.56, CI=0.32-0.96), and due to malignancy (HR=0.33, CI=0.16-0.69). Overall and cause-specific mortality was increased in both GH-replaced and non GH-replaced patients compared to general population controls, but mortality was generally highest in non GH-replaced patients.

Conclusion The present data from a national cohort of CO GHD patients does not support the suggestion that GH replacement is associated with increased mortality.

 

[slashlove]

I thought that HG does not give you cancer. However if you have cancer already can make grow faster....maybe I am wrong.


"Pain is temporary, Pride is forever»

 

[Michael Scally MD]

Carlzon D, Svensson J, Petzold M, et al. Insulin-like growth factor I and risk of incident cancer in elderly men – results from MrOS-Sweden. Clinical Endocrinology. http://onlinelibrary.wiley.com/doi/10.1111/cen.12962/abstract

Objective Studies of the association between circulating IGF-I and cancer risk have shown conflicting results. We have previously observed a U-shaped association between IGF-I and cancer mortality. The present study test the hypotheses of a U-shaped association between IGF-I and incident cancer.

Design Elderly men (2368), randomly recruited from the general community.

Methods IGF-I was measured in a cohort of elderly men. Complete data for incident cancer was obtained from the Swedish Cancer Registry. Statistical analyses included Cox proportional hazards regressions with or without a spline approach.

Results 369 participants had incident cancer after baseline. Prostate cancer was most frequent (n=140). There was no association between serum IGF-I and all cancer or prostate cancer incidence. However, there was a nonlinear association between IGF-I and non-prostate cancer incidence (p = <0.05). Exploratory analyses were performed for low and high serum IGF-I (quintiles 1 and 5) vs. intermediate (quintiles 2-4, referent). There was a tendency of increased non-prostate cancer risk in men with high IGF-I (HR = 1.26, 95% confidence interval (CI): 0.92-1.71, p=0.15). After excluding participants with follow-up of less than 2.6 years (half median follow-up time), to control for potential diagnostic delay, the association was statistically significant (HR = 1.55, CI: 1.03-2.35).

Conclusion There was a significant nonlinear association between IGF-I and non-prostate cancer. No association between IGF-I and prostate cancer was observed. Future studies are warranted to further investigate this nonlinear association, including whether IGF-I concentration is a reproducible, and useful, risk marker of non-prostate cancer.

 

[Dave202000]

Everyone has cancer cells at any given time our immunity mediates this and typically rids the body of these cells this is why u see a big correlation to those afflicted with cancer having a previous bout of lowered immunity also kaposis sarcoma in AIDS patients

 

[Dr JIM]

Child CJ, Conroy D, Zimmermann AG, Woodmansee W, Erfurth EM, et al. Incidence of Primary Cancers and Intracranial Tumour Recurrences in Growth Hormone-Treated and Untreated Adult Hypopituitary Patients: Analyses from HypoCCS. European Journal of Endocrinology. http://www.eje-online.org/content/early/2015/03/25/EJE-14-1123.abstract

Objective: Speculation remains that growth hormone (GH) treatment is associated with increased neoplasia risk. Studies in GH-treated childhood cancer survivors suggested higher rates of second neoplasms, while cancer risk data for GH-treated and untreated hypopituitary adults have been variable. We present primary cancer risk data from the Hypopituitary Control and Complications Study (HypoCCS) with a focus on specific cancers, and assessment of recurrence rates for pituitary adenoma (PA) and craniopharyngioma (CP).

Design: Incident neoplasms during HypoCCS were evaluated in 8418 GH-treated/1268 untreated patients for primary malignancies, 3668 GH-treated/720 untreated patients with PA history, and 956 GH-treated/102 untreated patients with CP history.

Methods: Using population cancer rates, standardised incidence ratios (SIRs) were calculated for all primary cancers, breast, prostate, and colorectal cancers. Neoplasm rates in GH-treated vs untreated patients were analysed after propensity score adjustment of baseline treatment group imbalances.

Results: During mean follow-up of 4.8 years, 225 primary cancers were identified in GH-treated patients, with SIR of 0.82 (95% confidence interval [CI] 0.71-0.93). SIRs (95% CI) for GH-treated patients were 0.59 (0.36-0.90) for breast, 0.80 (0.57-1.10) for prostate, and 0.62 (0.38-0.96) for colorectal cancers. Cancer risk was not statistically different between GH-treated and untreated patients (relative risk [RR]=1.00 ( 95% CI: 0.70-1.41) p=0.98). Adjusted RR for recurrence was 0.91 (0.68-1.22) p=0.53 for PA and 1.32 (0.53-3.31) p=0.55 for CP.

Conclusions: There was no increased risk for all sites, breast, prostate, or colorectal primary cancers in GH-treated patients during HypoCCS. GH treatment did not increase risk of PA and CP recurrences.

Those who have a family hx of "glandular CA" such as colon rectal, breast, prostate etc, must be ultra vigilant and undergo appropriate screening tests while GH is being supplemented bc although GH does NOT cause CA (genetics accomplishes that task for all intents and purposes) it can ACCELERATE the growth of such malignancies ONCE ESTABLISHED! (I'm NOT suggesting GH works in a selective manner!)

Another difference to consider is whether the supra-supraphysiologic doses and the duration of use practiced by PRO BB would alter the frequency of CA.

To that end DNA errors are a fact of life but few lead to significant physiologic derangement's for a variety of reasons. But the concern regarding GH, is in part, whether RAPIDLY REPLICATING "under GH's influence " have the time to institute those corrective measures necessary to delete the propagation of an abnormal or malignant cell line?

 

[Dr JIM]

....... clarification; 3rd line from the end of the last paragraph ....whether RAPIDLY REPLICATING ..... (insert) CELLS ....."under GH's influence"....