Safety of Mosanto's rBGH (Bovine Growth Hormone)

[Patrick S]

Forgive me if this has already been discussed, but the one study I could find that actually examined the relationship between dietary milk consumption and serum IGF-1 levels found no association whatsoever (Allan et al, 2002). Of course, its is serum concentrations that are most important, because IGF-1 can only have an effect if it makes it to the serum and from serum to cell-surface receptors. Their table 6 shows that those who drank no milk had serum IGF-1 levels not statistically different from those who drank 1/4pt, 1/2pt, or even 3/4pt of milk a day. Interestingly enough, however, their results did seem to indicate that soya milk did result in a significant increase in serum IGF-1. Allen et al (p. 1446) wrote:

Increasing dairy milk intake was not significantly associated with increasing serum IGF-I concentration in meat-eaters or vegetarians (Table 6) or among both groups combined (data not shown). However, vegan women who consumed 3⁄4 pint or more of soya milk/day had a significant 28% higher IGF-I concentration than vegan women who did not drink soya milk.

Allen et al, 2002. The Associations of Diet with Serum Insulin-like Growth Factor I and

Its Main Binding Proteins in 292 Women Meat-Eaters, Vegetarians, and Vegans. Cancer Epidemiology, Biomarkers & Prevention 11, 1441–1448,

[Patrick S]

. . . the FDA has said there's no significant difference between milk from treated & untreated cows, and no test can now distinguish between the two.

This bit is interesting. I'm a little surprised that there is no test that can tell the difference. Wouldn't a test for IGF-1 show a difference, per our discussion above?

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No.

Though there is a small difference in the average milk IGF-1 concentrations between rBGH-treated and non-rBGH-treated cows, the range of variation is very similar for both groups. The higher the IGF-1 in a sample, the more likely it came from a treated cow, but for most samples you'd simply have no way to know whether it came from a treated or an untreated cow.

According to the Joint FAO/WHO Expert Committee on Food Additives, the ranges of variation in milk IGF-1 concentration in untreated and treated cows are 1-9ng/ml, and 1-13ng/ml, respectively. Sources differ as to the average difference in IGF-1 from treated versus untreated cows, but most recent sources report the difference as being less than 4ng/ml.

By comparison, the concentration of IGF-1 in human milk is listed as 5-10ng/ml, and the concentraton of IGF-1 in adolescent human blood plasma is a whopping 180-780ng/ml -- somewhere between 13 and 780 times more rich in IGF-1 than milk from treated cows. And remember, the average differences in milk from treated vrs untreated cows is only a few ng/ml. . .

[docsconz]

Very interesting data, Patrick. This certainly helps give credance to the idea that direct human health effects of rBGH milk iare likely no different than non-rBGH milk. Of course that doesn't address issues of non-direct or environmental effects

looking at the human adolescent data, I can't help but wonder what those averages were like in generations past? I wonder if they are higher today could that be a causative factor for the increased incidence of diabetes? Obviously, this is likely to be a next to impossible study to do as I can not imagine that the data would be available for earlier generations or even testable.

[Patrick S]

looking at the human adolescent data, I can't help but wonder what those averages were like in generations past? I wonder if they are higher today could that be a causative factor for the increased incidence of diabetes?

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Luckily there are many ways to study the relationship between IGF-1 and diabetes that do not require a time machine. For instance, you can do a prospective study of individuals and determine whether or not IGF-1 levels predict subsequent development of diabetes. Or you could administer IGF-1 to diabetics and observe that effects on glucose metabolism/insulin sensitivity. I did a quick PubMed search and got over 1200 journal article references on the subject.

You're certainly correct in your view that there is a relationship between IGF-1 and diabetes; however the relationship appears to be the opposite of what you might think. That is to say, it appears that low plasma IGF-1, rather than high plasma IGF-1, is associated with increased risk of diabetes. I'll present a few representative examples of research, with quotes from the abstracts.

Qiu et al, 2005. Maternal plasma concentrations of IGF-1, IGFBP-1, and C-peptide in early pregnancy and subsequent risk of gestational diabetes mellitus. American Journal of Obstetrics and Gynecology 193(5):1691-7.

Free IGF-1 and IGFBP-1 were inversely associated with GDM risk. . . Women with free IGF-1 > or = 1.08 ng/mL experienced a 69% reduced risk of GDM (CI 0.12-0.75) compared with women having concentrations < 0.80 ng/mL. There was a 57% reduced risk of GDM among women with IGFBP-1 > or = 68.64 ng/mL (RR = 0.43, CI 0.18-1.05).

[NOTE: GDM is gestational diabetes, and IGFBP-1 is the IGF binding protein]

Ali and Pinkney, 2002. Therapeutic potential of insulin-like growth factor-1 in patients with diabetes mellitus. Treatments in Endocrinology 1(6):399-410.

The availability of recombinant human IGF-1 (rhIGF-1; mecasermin), used either alone or in combination with insulin, has led to experimental studies and clinical trials in humans testing these hypotheses. These studies have examined the impact of subcutaneous rhIGF-1 injections on sensitivity and metabolic parameters. In patients with type 1 and 2 diabetes mellitus, insulin sensitivity is significantly improved, insulin requirements are reduced, and glycemic control of dyslipidemia is generally improved in short-term studies. rhIGF-1 is a particularly attractive possibility in patients with type 2 diabetes mellitus, where insulin resistance is the fundamental problem. Some patients with genetic syndromes of severe insulin resistance also benefit from treatment with rhIGF-1, which can bypass blocks in the insulin signaling pathway.

Carroll et al, 1998. Recombinant human insulin-like growth factor-I (rhIGF-I) therapy in adults with type 1 diabetes mellitus: effects on IGFs, IGF-binding proteins, glucose levels and insulin treatment. Clinical Endocrinology 49(6):739-46.

. . .we examined the effects of 19 days' subcutaneous administration of rhIGF-I (50 micrograms/kg BID) on the levels of IGF-I, IGF-II and the IGF-binding proteins (IGFBPs), as well as the daily dose of insulin necessary to maintain glycaemic control in patients with type 1 diabetes mellitus. . .  The dose of insulin required for adequate glycaemic control decreased significantly during rhIGF-I therapy (46 +/- 7 vs. 31 +/- 8 U/day, P < 0.05, day -1 vs. day 19), as did the fasting free insulin concentration (8.4 +/- 1.5 vs. 5.0 +/- 0.8 mU/l, P < 0.05, baseline vs. day 5).

Dunger et al, 2003. Serum insulin-like growth factor-I levels and potential risk of type 2 diabetes. Hormone Research 60 Suppl 3:131-5.

Adult studies suggest that lower IGF-I levels at baseline predict increased risk for developing impaired glucose tolerance and type 2 diabetes.

Janssen and Lamberts, 2002. The role of IGF-I in the development of cardiovascular disease in type 2 diabetes mellitus: is prevention possible? European Journal of Endrocrinology 146(4):467-77.

Several observations suggest that there is a premature and progressive age-related decline in serum IGF-I bioactivity in type 2 diabetics, which eventually results in a (relative) IGF-I deficiency. In type 2 diabetics, close relationships have been demonstrated between glycaemic control and serum IGF-I levels, with worse control being associated with lower IGF-I levels.

[bunk]

a quick note: "rBGH is not a human hormone, therefore its effects on humans may not be the same as human growth hormone and are therefore somewhat unpredictable unless rigorously tested."

the first phrase is absolutely true.  in fact, rBGH has no effect on humans, partially because humans do not have receptors for it. 

Daughaday, W, Barbano DM. "Bovine somatotropin supplementation of diary cows." JAMA. 1990; 264:1003-1005

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Humans also do not have receptors for pesticides, yet some pesticides stimulate hormonal activities in humans despite the different molecular structures. The reason why is still unknown.

[jsolomon]

Humans also do not have receptors for pesticides, yet some pesticides stimulate hormonal activities in humans despite the different molecular structures. The reason why is still unknown.

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Eh?

We don't have caffeine receptors, but it still works on us. We may not understand the specifics, but they still bind to something that acts like a receptor. Unkown and unpredicted are two completely different things.

[Patrick S]

a quick note: "rBGH is not a human hormone, therefore its effects on humans may not be the same as human growth hormone and are therefore somewhat unpredictable unless rigorously tested."

the first phrase is absolutely true.  in fact, rBGH has no effect on humans, partially because humans do not have receptors for it. 

Daughaday, W, Barbano DM. "Bovine somatotropin supplementation of diary cows." JAMA. 1990; 264:1003-1005

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Humans also do not have receptors for pesticides, yet some pesticides stimulate hormonal activities in humans despite the different molecular structures. The reason why is still unknown.

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Humans, cows and indeed all mammals have receptors for GH (growth hormone), and it is known that many if not all of the effects of GH are receptor-mediated. For instance, we know that many of the effects of GH are caused by increasing IGF-1, and we know that the increase in IGF-1 production by the liver is a major receptor-mediated effect of GH, and is blocked by a GH receptor antagonist.

The reasons rBGH in milk has no effect on humans are, firstly, rBGH is not orally active (like most proteins it is destroyed by digestion --which is why cows receive rBGH via subcutaneous injection), and second, BGH is sufficiently different from HGH in its protein structure that it does not act as an agonist at human GH receptors. To use the lock and key analogy, the BGH 'key' does not fit the HG receptor 'lock.' Indeed, in the 1950's BGH injections were actually tried as a treatment for dwarfism, but the treatment had no effect whatsoever.