| LETTER
Milk hormone bashers are
all wet
". . .a direct effect of ingested IGF-1 is ruled out by the most elementary math." ". . . the claim that clinical research is 'non-animal' is patently false."
November 6, 2002
I am a molecular geneticist and
cell biologist whose present experiments fall entirely under the phony
classification of "non-animal alternatives" promoted by vegan and animal-rights
activists. My experience in statistics comes from my genetics background.
I have published in both the carcinogenesis and cancer cell biology fields,
and my 20 years of experience doing cell culture (which is neither non-animal
nor alternative) means that I know a fair amount about growth factors.
One of the gaping logical flaws in the tirades against milk is not covered on your Web site. These omissions and misrepresentations, championed most loudly by Robert Cohen, also are employed by Stephen Walsh, PCRM, and even Consumers Union. They are very effectively presented in Stephen Walsh's essay at: www.vegansociety.com/briefings/milkbreastcancer5.htm Before discussing Walsh's inaccuracies on the subject
of IGF-1, it is important to note that of the four cited above, Walsh is
the only one honest enough to report many of the data that do not support
the hypothesis that milk causes cancer. (See
Returning to Walsh's inaccuracies, he writes: CLA, calcium, and vitamin D have been hypothesised to give rise to a beneficial effect of dairy products. Insulin-like growth factor 1 (IGF-1) has been hypothesised to give rise to an adverse effect of dairy products.This appears to be a strategic omission, as higher IGF-1 levels also have been associated with multiple positive effects, including skeletal health and cognition (see references here, here, here, here, and here) . The former effect is the focus of a paper Walsh cites below, so he can't possibly be ignorant of it. High levels of IGF-1 in blood, or more specifically, a high ratio of IGF-1 to IGFBP-3 (insulin-like growth factor binding protein 3), have been associated with notably increased risk of premenopausal breast cancer, prostate cancer, colorectal cancer and lung cancer.Here, Walsh omits the well-known phenomenon of autocrine production of IGF-1 by tumor cells (see references here, here, here, and here), which by itself predicts an association, but the causation is in the opposite direction from the one Walsh peddles below. Put more simply, we already know that many tumors secrete their own IGF-1, which could account for the association, even long before diagnosis, because most tumors take years--some even decades--to grow to a size that allows detection. All cow's milk contains some IGF-1 and milk from cows treated with bovine growth hormone (sometimes referred to as BST) contains increased amounts of IGF-1.Increases are not always observed, and when they are, they are typically less than 2-fold. But this brings up a very important question that Walsh never addresses: how much IGF-1 does milk contain relative to the amount our bodies make each day? . . . .Adding about 600ml (three cups) of milk to the diet of adults aged 55 to 85 years caused an increase in IGF-1 levels from an average of 125 ng/ml to an average of 137 mg/ml [11]. . . .A direct effect of the IGF-1 in milk is not indicated by the existing evidence but cannot be entirely ruled out." [Editor's note: There was a typo in Stephen Walsh's paper which is repeated above. Instead of "137 mg/ml," the text should read "137 ng/ml."]This is pure hooey, because a direct effect of ingested IGF-1 is ruled out by the most elementary math. Guler et al. (Acta Endocrinol 1989, 121:753-8), using human subjects, calculated that the half-lives of free and carrier-bound IGF-1 were 10-20 and 20-30 minutes respectively. Therefore, they calculated that maintaining a constant level of IGF-1 involved the production of 10 mg per day (10,000,000 ng/day). Therefore, if one drinks 600 ml of milk containing 10 ng/ml IGF-1 (the range is incredibly wide), and all of it is absorbed intact (definitely not the case), the IGF-1 in milk would only increase the amount in your body by 6000 ng, or 0.06%. The idea that this increase may be biologically significant is preposterous. The idea that a 2-fold change in that miniscule increase (from rBGH treatment of cows) will be biologically significant is even more preposterous. Regardless of the mechanism, adding milk to the diet increases IGF-1 level.This is deceptive, since in the paper Walsh cited (Heaney et al., J. ADA 99:1228, 1999), subjects were merely told to add three 8-ounce servings of milk to their diets. Since the researchers explicitly noted that the milk group had a higher energy intake and gained weight, Walsh can't honestly claim that the increase was caused by milk--for all he knows, adding the same number of calories from avocados may produce the same or larger increase in serum IGF-1. This may lead to an increase in cancer risk.Anything's possible, but it's worth noting that it may lead to better bone health, growth, and cognition, too. The deceptive aspect of Walsh's approach is that he doesn't tell his audience anything about the well-known functions of IGF-1 as an essential mitogen--for scare value, he only presents it as a potential carcinogen. Mitogens signal cells to divide and are essential for growth, immune responses, wound healing, and many other processes. Carcinogens, with precious few exceptions, are substances that cause mutations. The underlying biology that is ignored by Walsh here is that cancer, in a nutshell, is a progressive genetic loss of responsiveness to signals that control cell division. The genetic changes (only some of which are inherited) known to play a role in cancer include those that cause growth factor receptors to be active in the absence of the growth factor, cause cells to secrete their own growth factors (the autocrine mechanisms ignored by the milk scaremongers), and inactivate components of programmed cell death and DNA repair machinery. Epigenetic factors such as mitogens have relatively little influence relative to these changes, and changes of 0.06% or even 10% obviously have even less potential influence. Walsh conveniently ignores most of the published literature on the known functions of IGF-1. For example, people with inherited deficits in IGF-1 production aren't healthy; mice that can't make any IGF-1 are usually dead. Here is a good review of much of the data in the online textbook of clinical genetics: www.ncbi.nlm.nih.gov:80/entrez/dispomim.cgi?id=147440 Walsh continues: The authors of the study leave as an open question whether the increase in IGF-1 in response to low-fat milk was due to conventional dietary factors, particularly protein, or to absorption of IGF-1 from the milk.Again, the last possibility is closed. An eighth-grader can do the math. . . . .Using milk to provide calcium entails accepting an accompanying increase in circulating IGF-1, probably due to increased protein and zinc intake, but possibly due to increased intake of IGF-1.Walsh simply can't tell whether the IGF-1 increase is caused by anything inherent to milk or merely by higher energy intake, and it is mathematically impossible for the intake of IGF-1 in milk to account for the increase in serum levels observed. Finally, for the benefit of those who promote the
political falsehood that animal research is wasteful and misleading, I
note that the data on digestion and protection (neither of which is complete)
of IGF-1 come from animal subjects (see references here,
here,
and here).
Another important note for those who claim that animals have rights is
that the measurements of IGF-1 in milk and human blood are done by methods
(ELISA or RIA) that require animal antibodies, which are produced by vivisecting
lab animals. This link
describes the use of ELISA for a slightly different test, such as HIV testing,
but the requirement for animal antibodies is the same. These experiments
demonstrate the falsehood of the categorical claim that clinical research
is "non-animal."
John A. Mercer, Ph.D.
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