Growth hormone therapy does not increase the risk of cancer

AlphaCog

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Growth hormone therapy does not increase, and even seems to lower the risk of cancer. This is evident from a meta-study published by Chinese endocrinologists at Zhejiang University College of Medicine in the Open Journal of Endocrine and Metabolic Diseases.

Growth hormone therapy does not increase the risk of cancer

Study
The researchers tracked 10 previously published studies that followed adults receiving growth hormone for several years. The subjects were diagnosed with adult growth hormone deficiency. So the studies may not say much about pharmacological athletes using growth hormone.

In the table below you will find more information about the studies used. Click on it for a larger version.
Growth hormone therapy does not increase the risk of cancer

Results
In the studies, the subjects who received growth hormone did not develop cancer more often than the subjects in the control groups. Growth hormone even reduced the risk of cancer.
Growth hormone therapy does not increase the risk of cancer

Growth hormone therapy does not increase the risk of cancer

The researchers found evidence of bias. This means that it seems that studies with less attractive results have not been published. However, the bias appeared to be modest, and the researchers suspect that the inclusion of the potentially missing studies in their meta-study would not really alter its outcome.

Conclusion
"Our study corroborates evidence from previous studies showing that growth hormone replacement therapy in adult growth hormone deficiency patients would not increase the risk of cancer; instead, it might be even decrease cancer risk", write the researchers.

"The results suggested that growth hormone replacement therapy in adult growth hormone deficiency patients was safe."

Source:
Open Journal of Endocrine and Metabolic Diseases 2017 January;7(9):173-89.
 
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AlphaCog

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Birdie

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This is an analysis of selected studies rather than a study.

The discussion says, "A doubtful association between GH replacement therapy and risk of developing cancer or recurrence of tumor has long been speculated." So it starts with the premise that the association is doubtful.

Interesting to see the Chinese groups that funded the study. Not that that in itself would negate it, but it seems likely to me this is an effort in favor of Big Pharma.
 
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AlphaCog

AlphaCog

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Growth hormone therapy does not alter the insulin-like growth factor-I/insulin-like growth factor binding protein-3 molar ratio in growth hormone-deficient children​

Abstract​

Background: Recent studies have linked raised levels of IGF-I and/or reduced levels of its main binding protein, IGF binding protein (IGFBP)-3, with the risk of developing cancer. A GH dose-dependent increase in IGF-I/IGFBP-3 molar ratio has been reported in subjects treated with GH, raising concern about the long-term safety.
Objective: The aim of this study was to evaluate changes in serum IGF-I, IGFBP-3, and IGF-I/IGFBP-3 molar ratio over the first 12 months of replacement GH therapy in GH deficient (GHD) children.
Methods: The study included 20 GHD children who had not previously received GH treatment, and 40 untreated non-GHD short children closely matched for age, gender, pubertal stage, and body mass index (BMI), as controls. Serum IGF-I, IGFBP-3 levels were measured before and after 12 months of GH treatment. Based on the molecular weight of IGF-I (7500) and IGFBP- 3 (40,000, mean of glycosylated variants), we calculated the molar ratio of IGF-I/IGFBP-3.
Results: IGF-I/IGFBP-3 molar ratio significantly increased during GH therapy (p=0.01). No significant difference in IGF-I/IGFBP-3 ratio was found between GHD children and controls at the different time points. In the multiple regression analysis, BMI (beta=0.33) and age (beta=0.33) proved to be the major predictors of the IGF-I/IGFBP-3 molar ratio (adjusted r2=0.53, p<0.0001).
Conclusions: Our results suggest that at a conventional replacement dose GH does not alter the IGF-I/IGFBP-3 molar ratio. Potential fears related to long-term cancer risk are likely to be greatest in patients exposed to high-dose GH therapy and with genetic predisposition to high IGF-I and/or low IGFBP-3 concentrations.
 
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@AlphaCog Is there a correlation with the increase in estrogen because from what we read in here they are agonists with each other?
 
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AlphaCog

AlphaCog

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@AlphaCog Is there a correlation with the increase in estrogen because from what we read in here they are agonists with each other?
Found some interesting research:

Estrogen treatment for acromegaly

Abstract

Estrogens have been used in patients with acromegaly since the 1930-1940s, suppressing plasma IGF-1 levels and improving clinical signs and symptoms of acromegaly. Estrogens antagonize GH function at the post-receptor level, inhibiting GH signaling, thus decreasing GH-induced hepatic IGF-1 synthesis. We report our experience with four female patients with active acromegaly, naïve to medical treatment or inadequately controlled by somatostatin receptor ligands (SRLs) or the GH-receptor antagonist. Adding estrogen treatment (contraceptive pills or transdermal estrogen patches) to their ongoing medical treatment, suppressed IGF-1 significantly in all patients, achieving hormonal remission in three of them. We review the available data on the use of estrogens and selective estrogen receptor modulators in acromegaly, and their mechanisms of action. Estrogens could be an alternative, inexpensive adjuvant treatment for females with active acromegaly, who are only partially responding to SRLs or to the GH-receptor antagonist.

Estrogens and selective estrogen receptor modulators in acromegaly

Abstract

Despite recent advances in acromegaly treatment by surgery, drugs, and radiotherapy, hormonal control is still not achieved by some patients. The impairment of IGF-1 generation by estrogens in growth hormone deficient patients is well known. Patients on oral estrogens need higher growth hormone doses in order to achieve normal IGF-1 values. In the past, estrogens were one of the first drugs used to treat acromegaly. Nevertheless, due to the high doses used and the obvious side effects in male patients, this strategy was sidelined with the development of more specific drugs, as somatostatin receptor ligands and dopamine agonists. In the last 15 years, the antagonist of growth hormone receptor became available, making possible IGF-1 control of the majority of patients on this particular drug. However, due to its high cost, pegvisomant is still not available in many centers around the world. In this setting, the effect of estrogens and also of selective estrogen receptor modulators on IGF-1 control was reviewed, and proved to be an ancillary tool in the management of acromegaly. This review describes data concerning their efficacy and place in the treatment algorithm of acromegaly.

Mechanism of estrogenic action in acromegaly

Abstract
In four acromegalic patients, estrogen therapy did not significantly alter the mean values of basal radioimmunoassayable plasma growth hormone. In two patients, estrogen therapy did not qualitatively alter the lack of reduction of plasma growth hormone levels after oral administration of glucose, nor did it reduce in these patients the response of plasma growth hormone to insulin-induced hypoglycemia. In one of the patients, insulin sensitivity with respect to glucose and the hypoglycemia-induced growth hormone rise seemed greater during estrogen therapy. Despite the absence of demonstrable reductions inplasma growth hormone level under varying experimental circumstances, the administration of estrogen resulted in reduction of urinary calcium and hydroxyproline excretion, in reduction of radiocalcium bone accretion rates and exchangeable pools, in reduction of serum phosphorus, and in more negative nitrogen balances. The experimental data therefore suggest that estrogen may be a peripheral antagonist of the effects of excessive growth hormone secretion in acromegaly.
 
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@AlphaCog Thanks, so according to this study they don't seem to reinforce each other but act as antagonists 👍
 
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