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The War on Milk – GM Dairy and Cancer Links

Brandon Turbeville
Activist Post

Wednesday, May 18, 2011

I wrote an article recently detailing the impacts of rBGH on the welfare of dairy cows. I explained how the use of rBGH was responsible for increased rates of mastitis and how rBGH injections actually have the potential to decrease milk production. Yet, aside from the damage to the animals, rBGH usage is significant in that it also affects humans consuming the milk.

This is because Insulin Growth Factor 1 (IGF-1), another powerful hormone increased in the animals’ system by injections of rBGH, lingers in the milk and has been linked to breast, colon, and prostate cancer in humans.[1]

IGF-1 is present naturally in both cows and humans, and is important for mediating cellular response to growth hormones. While the growth hormones themselves are quite different, cow and human IGF-1 are identical to one another.[2]

Humans consume their own IGF-1 which is digested in the stomach and, obviously, is harmless. However, the IGF-1 present in cow milk, especially that which comes from animals that were treated with rBGH survives digestion and moves to the intestinal tract. [3]  This is due to the fact that the IGF-1 produced in human saliva is free IGF-1 and is digested by the stomach. The IGF-1 in cow milk however, is protected from digestion by the milk protein casein and bypasses the digestive process.[4]
There have been many studies have shown a definite link between increased IGF-1 levels and breast, colon, and prostate cancer. Herbert Yu and Thomas Rohan addressed this in their study “Role of the Insulin-like Growth Factor Family in Cancer Development and Progression.” In their conclusion they state:

Laboratory experiments demonstrate that IGF’s are able to stimulate the growth of a wide variety of cancer cells and to suppress apoptosis. In addition to their direct effects on cancer cells, IGF’s also interact synergistically with other mitogenic molecules and counteract antiproliferative molecules that are involved in cancer development and progression. Findings of experimental studies are supported by the observations of epidemiologic studies, which have shown that elevated levels of IGF-1 in the circulation are associated with increased risk for several common cancers.[5]

The National Institute of Health (NIH) conference discussion entitled “Insulin-like Growth Factors and Cancer,” which was published in the Annals of Internal Medicine in 1995, explains the connection a bit further. Here it is stated:

As could be predicted from the importance of IGF’s, their binding proteins, and their receptors in normal cellular growth and development, it has become apparent over the past few years that IGF’s are important mitogens in many types of malignancies. Although these conclusions were initially derived from in vitro studies, IGF’s may enhance in vivo tumor cell formations, growth, and even metastasis. Insulin-like Growth Factors may reach tumors from the circulation (endocrine) or as a result of local production by the tumor itself (autocrine) or by adjacent stromal tissue (paracrine). Tumors also express many of the IGF-binding proteins, which modulate IGF action, and IGF receptors, which mediate the effects of IGF’s on tumors. We highlight important aspects of IGF’s in normal cell growth and their role in certain malignancies.[6]

Essentially, the evidence is becoming clearer and clearer that IGF’s (IGF-1, IGF-2, insulin) play an important role in the development and spread of many different forms of cancers.[7]

In relation to breast, colon, and prostate cancer, it is well known that increased levels of estrogen can be a major cause. This is the reason why the improper and overuse of soy products is such a problem and why they are implicated in the increase in these forms of cancers, as well as the physical “feminizing” of young men and the early development of young girls.

While neither increased soy nor increased IGF-1 is likely the sole cause of these cancers, they are most definitely a major factor, and they apparently work in tandem with one another. Much of the scientific evidence shows that IGF-1 encourages the proliferation of excess estrogen, while at the same time encouraging tumor growth. Dr. LeRoith addresses this at the same NIH conference listed above when he says:

Many cancers, especially those developing in the post-menopausal period, express estrogen and progesterone receptors. . . . . . In addition to classic hormones, several growth factors including transforming growth factors, epidermal growth factors, and IGF’s, have been shown to be involved in breast cancer. . . . . . Estrogen receptor-positive tumors will thus respond to antiestrogens such as tamoxifen, which is widely used clinically. Initially, it was thought to affect cancer cells primarily by blocking the activation of estrogen receptors; it has also been shown, however, to decrease circulating IGF-1 levels in women with breast cancer and may thus prove effective in treating both estrogen receptor-positive and estrogen receptor-negative cancers. Another agent that inhibits the proliferation of breast cancer cells is retinoic acid and its derivatives. . . . . . The mechanism by which retinoids affect the IGF-induced growth of breast cancer cells seems to involve modulation of local IGF-binding protein production; specifically, retinoic acid may also reduce circulating IGF-1 levels and may thus affect tumor growth in vivo by more than one mechanism. The above data suggest that IGF’s are likely to be involved in breast cancer at the level of tumor growth and perhaps at the level of initial development and later metastases. Ongoing studies involve attempts to interfere with the IGF system to develop additional therapeutic regimens.[8]

In effect, Dr. LeRoith is showing that IGF-1 can play a major role in breast cancer due to the fact that breast cancer cells react quite strongly in its presence.  This is also evidenced by the fact that many doctors have recognized this connection and are trying to treat breast cancer through reducing and manipulating IGF levels. But if IGF levels do not cause cancer directly, they still can play a major role in promoting its growth through increase in estrogen.

This applies to colon and prostate cancer as well.

With respect to colon cancer, for instance, it has been shown that IGF-1 receptors are found throughout the intestines with most of those receptors existing in the colon. In a study published in the British Journal of Cancer, it was found that 5 out of the 8 human colorectal cancer cell lines responded to IGF-1.  Indeed, IGF-1 increased growth in the cancerous cells by as much as 3-fold.[9] Furthermore, past studies have offered evidence which may suggest that colon carcinoma tumors produce IGF-1 on their own for the purposes of stimulating their own growth.[10] When taken together, this evidence helps to understand how increased levels of IGF-1 contribute to colon cancer.

However, colon, breast, and prostate cancers are not the only diseases associated with IGF-1. Osteosarcoma, a type of bone cancer, as well as lung cancer has been linked to IGF-1. In the same NIH conference listed above, Dr. Lee Helman states:

Osteosarcoma is the most common bone tumor in children, usually occurring during the adolescent growth spurt at sites of rapid bone growth. Because IGF-1 was initially described as the factor produced in the liver that directly mediated the effect of growth hormone on skeletal growth, there has been interest in a potential role for IGF-1 in the pathogenesis of osteosarcoma. Support for a role for IGF-1 in osteosarcoma growth comes from data showing that IGF-1 is a potent mitogen for human osteogenic sarcoma cells. Further, several reports have shown that a rat chondrosarcoma ( a closely related tumor) and a murine osteosarcoma are growth-inhibited in animals that have had hypophysectomy, presumably through the inhibition of the growth hormone – IGF axis. . . . . . It therefore appears that the growth hormone – IGF-1 axis may play a role in the unregulated proliferation of osteosarcoma tumor cells and that blocking of this axis using somatostatin analogs that reduce the circulating levels of growth hormone and IGF-1 may have therapeutic potential.[11]

IGF-1 is also known to play a role in lung development, and for that reason has been implicated as a cause in some forms of lung cancer. Another study published in the British Journal of Cancer in 1992 makes this clear. It says:

Thus IGF’s seem to be important in lung development and are also implicated in growth regulation of lung tumors. Primary lung tumors possess IGF-1 binding sites as shown by autoradiography, with the highest density of receptors in squamous cancers and small cell lung cancer. . . . . Thus there is good evidence that lung cancer cells produce IGF-1 and IGF BP’s, express IGF binding sites and exhibit a mitogenic response to exogenous IGF-1, suggesting that IGF-1 can function as an autocrine growth factor for lung cancer. [12]

Indeed, with the evidence cited above, and with no lack of scientific studies which corroborate the link between IGF-1 and cancer, there is no logical reason as to why anyone would consume or approve a product like rBGH in dairy milk. Yet, as will be discussed in a future article, the FDA has not only promoted the hormone, but it has actually moved to try and prevent consumers from being able to avoid it. While its initial attempt may have failed, recent attacks launched on raw milk producers should serve as a warning sign that the freedom to choose wholesome and healthy foods will not be respected by the FDA.

Sources:


[1] “rBGH: How Artificial Hormones Damage the Dairy Industry and Endanger Public Health.” Food and Water Watch. http://www.foodandwaterwatch.org/food/report/rbgh-how-artificial-hormones-damage-the-dairy-industry-and-endanger-public-health-2/rbgh-how-artificial-hormones-damage-the-dairy-industry-and-endanger-public-health-1/ Accessed May 24, 2010.
[2]  Hansen, Michael, Ph.D., Halloran, Jean M., Groth, Edward III, Ph.D., Lefferts, Lisa Y.“Potential Public Health Impacts Of The Use of Recombinant Bovine Somatotropin In Dairy Production.” ConsumersUnion.org. September 1997. http://www.consumersunion.org/pub/core_food_safety/002272.html Accessed May 24, 2010.
[3]  “rBGH: How Artificial Hormones Damage the Dairy Industry and Endanger Public Health.” Food and Water Watch. . http://www.foodandwaterwatch.org/food/report/rbgh-how-artificial-hormones-damage-the-dairy-industry-and-endanger-public-health-2/rbgh-how-artificial-hormones-damage-the-dairy-industry-and-endanger-public-health-1/ Accessed May 24, 2010.
[4] Hansen, Michael Ph.D., Halloran, Jean M., Groth, Edward III, Ph.D., Lefferts, Lisa Y. “Potential Public Health Impacts Of The Use Of Recombinant Bovine Somatropin In Dairy Production.”  Consumersunion.org. September 1997. http://www.consumersunion.org/pub/core_food_safety/002272.html Accessed May 24, 2010.
[5]  Rohan, Thomas, Yu, Herbert. “Role of the Insulin-like Growth Factor Family in Cancer Development and Progression.”  Journal of the National Cancer Institute. September 20, 2000. 92 (18). 1472-1489. http://www.ncbi.nlm.nih.gov/pubmed/10995803 Accessed May 24, 2010.
[6] LeRoith, Derek; Baserga, Renato; Helman, Lee; Roberts, Charles T. “Insulin-like Growth Factors and Cancer.”  Annals of Internal Medicine. January 1, 1995. Vol. 122. No.1. Pp. 54-59. http://www.annals.org/content/122/1/54.full Accessed May 24, 2010.
[7]  Hansen, Michael Ph.D., Halloran, Jean M., Groth, Edward III, Ph.D., Lefferts, Lisa Y. “Potential Public Health Impacts Of The Use Of Recombinant Bovine Somatropin In Dairy Production.” ConsumersUnion.org. September 1997. http://www.consumersunion.org/pub/core_food_safety/002272.html Accessed May 24, 2010.
[8] LeRoith, Derek; Baserga, Renato; Helman, Lee; Roberts, Charles T. “Insulin-like Growth Factors and Cancer.”  Annals of Internal Medicine. January 1, 1995. Vol. 122. No.1. Pp. 54-59. http://www.annals.org/content/122/1/54.full Accessed May 24, 2010.
[9]  Lahm, H; Suardet, L; Laurent, PL; Fischer, JR; Ceyhan, A; Givel, JC; Odartchenko, N. “Growth regulation and co-stimulation of human colorectal cancer cell lines by insulin-like growth factor I, II and transforming growth factor.” British Journal of Cancer, 65,  341-346. 1992.  http://www.ncbi.nlm.nih.gov/pubmed/1558785 Accessed May 24, 2010.
[10] Tricoli, James V; Rall, Leslie B; Karakousis, Constantine P; Herrera, Lemuel; Petrelli, Nicholas J; Bell, Graeme I; Shows, Thomas B.  “Enhanced Levels of Insulin-like Growth Factor Messenger RNA in Human Colon Carcinomas and Liposarcomas.” Cancer Research 46, 6169-6173, December 1986. http://cancerres.aacrjournals.org/cgi/content/abstract/46/12_Part_1/6169 Accessed May 24, 2010.
[11] LeRoith, Derek; Baserga, Renato; Helman, Lee; Roberts, Charles T. “Insulin-like Growth Factors and Cancer.”  Annals of Internal Medicine. January 1, 1995. Vol. 122. No.1. Pp. 54-59.
[12] McCauley, V.M. “Insulin-like growth factors and cancer.” British Journal of Cancer 65, 311-320. 1992. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1977607/ Accessed May 24, 2010.

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