In short: IGF-1 itself is not an oncogene (i.e., it does not cause cancer directly), but it acts as a powerful stimulator of cell growth and survival. This means that it can significantly accelerate the development of pre-existing cancers and possibly contribute to their occurrence.
1. How does IGF-1 work normally?
IGF-1 is a hormone similar in structure to insulin. Its main physiological role is:
Stimulation of cell growth and division (proliferationProliferation is the process of cell multiplication, increasing tissue volume. It underlies the growth and differentiation of tissues during individual development, ensures the renewal of cells and intracellular structures. Cell proliferation is a process by which a cell grows and divides to form two daughter cells.).
Preventing programmed cell death (apoptosis).
Stimulation of anabolism (growth of muscle and bone tissue).
These functions are absolutely normal and necessary for the growth of the body in childhood and the maintenance of tissues in adults.
2. Why is IGF-1 associated with oncogenic risk?
The problem arises when these powerful stimulating properties of IGF-1 act on precancerous or cancerous cells.
‘Fuel’ for the tumor: Many types of cancer cells (for example, in breast, prostate, colon, and lung cancers) have IGF-1 receptors (IGF-1R) on their surface. Binding of IGF-1 to these receptors activates intracellular signaling pathways (primarily PI3K/Akt and MAPK/Erk), which:
They force the cell to divide uncontrollably.
Inhibit apoptosis, allowing cancer cells to avoid death.
They stimulate the formation of new blood vessels (angiogenesis) that feed the tumor.
May contribute to metastasis.
Synergy with other oncogenes: IGF-1 can enhance the action of known oncogenes (for example, mutant Ras or MYC).
Reduced treatment effectiveness: High levels of IGF-1 may make some tumors less sensitive to chemotherapy and radiation therapy.
3. How high is the risk? Key points
Balance and context: The risk depends not only on the level of IGF-1, but also on the level of its main binding protein — IGFBP-3. .High levels of IGF-1 combined with low levels of IGFBP-3 are associated with an increased risk of several types of cancer.
Not the ’cause’, but the ‘catalyst’: Most studies indicate that IGF-1 does not cause cancer from scratch, but rather promotes the growth and progression of pre-existing micro-tumors, which many people have but are usually destroyed by the immune system.
Dose and duration: Long-term elevated IGF-1 levels (hyperproduction) are associated with a higher risk. A single exposure is not likely to pose a significant threat to a healthy person.
4. Where does elevated IGF-1 come from?
Endogenous (internal): The main stimulator of IGF-1 production in the liver is growth hormone (somatotropin). High levels of growth hormone (such as in acromegaly) directly lead to high IGF-1 and significantly increase the risk of cancer.
Exogenous (external):
Food: A diet high in animal protein and dairy products may moderately increase IGF-1 levels.
Supplements and preparations:This is the main area of concern.
Recombinant Human IGF-1: Used in research, but not approved for widespread clinical use. Its use without strict medical indications is extremely dangerous because of its oncogenic potential.
IGF-1 boosters (for example, Deer Antler Velvet): Some supplements that are popular in the sports community claim the ability to increase IGF-1 levels. Their effectiveness is often not proven, and the potential risk is not studied.
Growth Hormone (HGH): Because it directly increases IGF-1 levels, its uncontrolled use also carries cancer risk.
Conclusion
IGF-1 is a two- faced hormone. on the one hand, it is vital for normal growth and metabolism. On the other hand, its ability to stimulate cell division and survival makes it a potential cancer ally.
Thus, the oncogenic risk of IGF-1 lies not in its direct carcinogenicity, but in its role as a powerful growth stimulator that can ‘fuel’ the development of a tumor.
In short: IGF-1 itself is not an oncogene (i.e., it does not directly cause cancer), but it acts as a powerful stimulator of cell growth and survival. This means it can significantly accelerate the progression of existing cancers and potentially contribute to their onset.
1. How does IGF-1 work normally?
IGF-1 is a hormone structurally similar to insulin. Its primary physiological roles are:
Stimulating cell growth and division (proliferation).
Inhibiting programmed cell death (apoptosis).
Stimulating anabolism (growth of muscle and bone tissue).
These functions are entirely normal and necessary for body growth in childhood and for tissue maintenance in adults.
2. Why is IGF-1 associated with oncogenic risk?
The problem arises when these powerful stimulatory properties of IGF-1 act on pre-cancerous or cancerous cells.
‘Fuel’ for the tumor: Many types of cancer cells (e.g., in breast, prostate, colorectal, and lung cancer) have IGF-1 receptors (IGF-1R) on their surface. The binding of IGF-1 to these receptors activates intracellular signaling pathways (primarily PI3K/Akt and MAPK/Erk), which:
Cause the cell to divide uncontrollably.
Suppress apoptosis, allowing cancer cells to evade death.
Stimulate the formation of new blood vessels (angiogenesis), which nourish the tumor.
Can promote metastasis.
Synergy with other oncogenes: IGF-1 can enhance the action of known oncogenes (e.g., mutant Ras or MYC).
Reduced treatment efficacy: High levels of IGF-1 can make some tumors less sensitive to chemotherapy and radiation therapy.
3. How high is the risk? Key points
Balance and context: The risk depends not only on IGF-1 levels but also on the level of its main binding protein, IGFBP-3. High levels of IGF-1 combined with low levels of IGFBP-3 are associated with an increased risk of several cancers.
Not a ’cause,’ but a ‘catalyst’: Most research indicates that IGF-1 does not cause cancer from scratch, but rather promotes the growth and progression of microtumors that have already arisen, which are present in many people but are usually eliminated by the immune system.
Dose and duration: Chronically elevated levels of IGF-1 (hyperproduction) are linked to a higher risk. A single exposure is unlikely to pose a significant threat to a healthy person.
4. What causes elevated IGF-1?
Endogenous (internal): The main stimulator of IGF-1 production in the liver is growth hormone (somatotropin). High levels of growth hormone (e.g., in acromegaly) directly lead to high IGF-1 and significantly increase cancer risk.
Exogenous (external):
Diet: A diet high in animal protein and dairy products can moderately increase IGF-1 levels.
Supplements and drugs: This is the primary area of concern.
Recombinant human IGF-1: Used in research but not approved for broad clinical use. Its use without strict medical indications is extremely dangerous due to its oncogenic potential.
IGF-1 boosters (e.g., Deer Antler Velvet): Some supplements popular in sports circles claim to boost IGF-1 levels. Their efficacy is often unproven, and their potential risk is unstudied.
Growth Hormone (HGH): Since it directly increases IGF-1 levels, its uncontrolled use also carries an oncological risk.
Conclusion
IGF-1 is a double-edged sword. On one hand, it is vital for normal growth and metabolism. On the other hand, its ability to stimulate cell division and survival makes it a potential ally of cancer.
Thus, the oncogenic risk of IGF-1 lies not in its direct carcinogenicity, but in its role as a powerful growth stimulant that can ‘fuel’ tumor development.
