Human Growth Hormone Igf1 and Cancer

As a result of studies indicating GH may have the ability to restore a more youthful physiology and enhance the quality of life the benefits of human growth hormone (GH, also known as human growth hormone or hGH) have received increasing attention from not only the media but the medical profession as well.

However, there is controversy centered on the possibility that maintaining youthful GH levels may actually be harmful in the long run and may result in shortening life span by inducing cancer.

Intuitively, it is obvious that naturally occurring endogenous GH released within physiological parameters itself could not possibly cause cancer. The reasoning for this statement is actually quite simple because all mammalian species achieve the maximum level of GH levels when reaching late adolescence and young adulthood. If endogenous GH were actually a cause of cancer, then all mammalian species including man would have the highest incidence of cancer during late adolescence and young adulthood. However, as we all know, this is not what occurs.

So, what then causes cancer? The answer unfortunately, is more than a little involved. We know that a minimum of 75% of all cancers have been shown to have environmental etiologies. In addition, there are certain factors that predispose individuals to have a higher propensity to develop uncontrolled cellular proliferation and induce the suppression of apoptosis, leading to oncogenesis or the formation of cancer. In addition, we know that the incidence of cancer generally occurs later in life as opposed to late adolescence and young adulthood when we have the highest levels of GH.

The first foundational objective essential to gaining an insight into these issues is to clearly understand the hypothalamic-pituitary axis. More often than not, we forget the physiological safety mechanisms designed within our systems to protect us. In this case, we refer to the negative inhibitory feedback loop designed to decrease or stop the release of endogenous GH when levels exceed the physiological range. This inhibitory feed back loop plays a significant role in the hypothalamic-pituitary axis and realizing its significance is vital to understanding the advantages of using growth hormone releasing hormone (GHRH) to increase endogenous GH as opposed to using exogenous GH.

This will lead to the discussion of why assessing increases in insulin-like growth factor type1 (IGF-1) as a marker of GH efficacy may not only be unreliable, but a compelling argument will be presented that the practice may be nothing more than the perpetuation of a medical myth. In fact, conclusive data from multiple sources showing that increases in IGF-1 are conducive to the propagation of oncogenesis will be presented and then supported by published research. This conclusion is very well supported by scientific observation, clinical data, and published research, as well as being supported by general physiological concepts – all of which will be presented later in this chapter.

Finally, the inter-relationship between GH, GHRH, and IGF-1, as well as how each individual component correlates with incidence of cancer, will be thoroughly explained. It is important however, to first discuss the common characteristics of cancer and the various treatment options available so that all readers have the same foundational knowledge essential to understanding and conceptually comprehending the material being presented.

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