Excess growth hormone secretion causes a condition known as acromegaly, and is associated with an increase in soft tissues, edema and joint pain. Supraphysiologic growth hormone levels also decrease apoptosis, the protective process of finding abnormally growing cells or early tumors. Since high levels of growth hormone can inhibit apoptosis and because it is an anabolic hormone which makes tissues grow (including cancer cells, potentially), questions have been raised about HGH replacement therapy as a cause of cancer. Individuals with acromegaly have supra- physiologic levels of HGH, and they have an increased risk for colon cancer. However, acromegaly confers an all-cancer risk of just 0.76.
The New England Journal of Medicine, October 1999, concluded, “There is no evidence that HGH replacement therapy affects the risk of cancer or cardiovascular disease.” Much higher-than-normal levels of HGH in conjunction with low levels of another protein known as IGF-1-BP-3 (IGF binding proteins) may have a role in cancer risk development (prostate, breast and colo-rectal), according to the Lancet, April 2004.
IGF-1-BP-3 appears to have an inhibitory effect on cell growth, helping protect one from cancer by promoting programmed cell death, called apoptosis. IGFBP-3 inhibits mitogenesis by sequestering IGF-1 from the type 1 IGF receptor. It also modulates retinoid receptors, interacts with TGF-beta, and blocks cell division at G2/M. The journal Cancer reported in 2005 that “IGF-1 was not associated positively with the risk of prostate carcinoma; however an increase in the IGFBP-3 level was associated with a modest decrease.” Appropriate HGH replacement therapy tends to produce a greater rise in IGF-BP3 then IGF-1. Close monitoring of IGF-1 and IGF-BP3 levels during replacement therapy is essential to avoid exceeding optimal and physiologic ranges.
Abnormally high levels of growth hormone are also associated with increased production of various inflammatory agents such as leukotrienes and cytokines. Any overproduction of inflammatory compounds resulting in an imbalance of the ratio of inflammatory to anti-inflammatory compounds causes silent inflammation, which is at the root of most aging-related diseases. Therefore, any HGH replacement program must avoid causing supraphysiologic growth hormone levels and should be balanced with other lifestyle interventions known to prevent and treat silent inflammation.
“Insulin-Like Growth Factor-1 is a Vascular Protective Factor,” an article published in a 2004 issue of the American Heart Association journal, Circulation is one of many shedding light on the importance of maintaining optimal levels of growth hormone and other hormones for keeping our physiology functioning at its highest level. The following quote, from the first paragraph, of the article states the message clearly: “Recent advancements in cardiology have focused on proliferation and regeneration as a potential cardiovascular defense mechanism. Within this framework, growth factors are acquiring increasing importance; insulin-like growth factor-1 (IGF-1) emerges among them for its versatile pleiotropic actions.” The authors concluded with the following statements:
• “Increasing evidence indicates…that IGF-1 protects against endothelial dysfunction, atherosclerotic plaque development, the metabolic syndrome, clinical instability, and ischemic myocardial damage.”
• “Measurement of circulating IGF-1 may add valuable information to the current assessment of cardiovascular risk. Individuals with traditional cardiovascular risk factors but normal or elevated IGF-1 may be protected, at least in part, against disease. With reduced IGF-1 levels, instead, vascular risk factors may fully exert their detrimental effects, through unopposed endothelial dysfunction, endothelial apoptosis, and development of unstable plaques. Those with markedly reduced IGF-1 might develop disease even in the absence of traditional risk factors. It is worth noting that healthy centenarians have high serum IGF-1 concentrations.”
