Yet another paper from Poland, this one published in the peer-reviewed international Journal of Pediatric Gastroenterology and Nutrition,(1) is providing insights about bovine (cow) casomorphins finding their way into the blood of babies via human milk. This time the casomorphin is BCM5, which is derived from the breakdown of BCM7, which in turn is derived from A1 beta-casein. Until now I have largely ignored bovine BCM5, and in my book ‘Devil in the Milk” I only mentioned it once (p38). (2) But I can see that in future I am going to have to look at it much more closely.
Those of us that are interested in casomorphins and human health have known for a long time that bovine BCM5 is a more powerful opioid than bovine BCM7. One paper makes the comparison that whereas bovine BCM7 is similar in opioid strength to morphine, bovine BCM5 is ten times more powerful than either.(3) However, the accepted evidence has been that it is probably not released by digestion of cow milk in the human gut, whereas BCM7 was definitely released.(4, 5)
What the Polish work is indicating is that even if BCM5 is not normally found in the human gut
(and there is a logic why that might be so, related to the DPP4 enzyme that is needed to break down BCM7 to BCM5 only being found within the gut on mesenteric cells, rather than circulating freely in the gut), BCM5 is getting formed from BCM7 in the sera (blood) (where DPP4 does circulate freely) or other tissues. From there it is getting transferred into human milk. From there it gets into the stomachs and blood of babies.
[Update August 2016: On re-reading this post I see that some material above (which I have now struck out) was incorrect. Although DPP4 does break down BCM7, it does this by fracturing the peptide at the N terminus between the second and third amino acids of the peptide. The enzyme previously identified in the literature as being capable of breaking down BCM7 to BCM5 is carboxypeptidase Y which acts on the carboxyl end of the peptide. This correction has no implications for the rest of the post]
If all of this is true – and that is what this latest research is indicating – then the implications are huge.
So what did this Polish research actually report?
The study is reported as a case study of a child suffering bouts of apnoea immediately after breast feeding. But there is much more to it than that, and it is really a case-control with 10 normal babies as the controls. I am actually more interested in the findings from the controls, but first the case itself.
The mother self diagnosed that the baby was suffering from the apnoea on those occasions when she (the mother) had been drinking large quantities of cow milk. Sure enough, on testing the baby’s blood, extremely high levels of bovine BCM5 were found. (For those that think quantitatively, 15,147 ng/mL.). Other possible causes of the apnoea were investigated but proven negative. So this in itself does not prove causation. But the association (which in science is not quite the same thing as ‘proof’) is a remarkable finding and points in only one direction.
So how does this level actually compare to the levels found in the normal babies? In these babies it was much lower, ranging from 1 ng to 864 ng/mL. Accordingly, there is a remarkable contrast between the controls and the case, with the case being an extreme outlier.
However, my interest is in the fact that for seven out of eight of the controls (data for the other two is not presented, which is frustrating), considerable levels of BCM5 were found. For the eighth control which had only 1 ng/mL, the mother did not like cow milk and did not drink it, whereas all of the other mothers did. These babies were aged 7-14 weeks and all were exclusively breast-fed. To reiterate, although much lower than for the case, the levels in these controls are still high.
So here we have evidence of considerable levels of BCM5 getting into babies blood via their mothers’ milk. This is a remarkable finding, although highly consistent with other work of this group that showed BCM7 was getting through to babies via their mothers’ milk.(6)
Once again we can be confident that the mainstream dairy industry will denigrate this research. They will probably point out that it is only a case study (although actually it is a case-control). And they will point out that the authors themselves emphasise that further work is needed including measuring the BCM5 in the milk of the mothers, and taking blood readings at different times relative to feeding times.
However, what this research does do is throw light into a number of previously dark places. BCM5 is now looking more important than previously, and this paper does provide confirmatory evidence that nasty peptides can get from cows’ milk to human babies via their mother’s’ milk. What Mum eats and drinks is important for baby. If Mum drinks milk containing A1 beta-casein, then it would seem that baby is gong to drink casomorphins.
1. Wasilewska J, Kaczmarski M, Kostyra E, Iwan M. Cow’s-milk-induced Infant Apnoea With Increased Serum Content of Bovine beta-Casomorphin-5. J Pediatric Gastroenterology and Nutrition. 2011 June; 52(6): 772-775
2. Woodford K. Devil in the Milk: Illness, Health and Politics: A1 and A2 Milk. Wellington New Zealand: Craig Potton Publishing 2007.
3. Hedner J, Hedner T. beta-Casomorphins induce apnea and irregular breathing in adult rats and newborn rabbits. Life Sci. 1987 Nov 16;41(20):2303-12.
4. De Noni I. Release of b-casomorphins 5 and 7 during simulated gastro-intestinal digestion of bovine b-casein variants and milk-based infant formulas. Food Chemistry 2008 110(4):897-903.
5. Svedberg J, de Haas J, Leimenstoll G, Paul F, Teschemacher H. Demonstration of beta-casomorphin immunoreactive materials in in vitro digests of bovine milk and in small intestine contents after bovine milk ingestion in adult humans. Peptides. 1985 Sep-Oct;6(5):825-30.
6. Wasilewska J, Sienkiewicz-Szlapka E, Kuzbida E, Jarmolowska B, Kaczmarski M, Kostyra E. The exogenous opioid peptides and DPPIV serum activity in infants with apnoea expressed as apparent life threatening events (ALTE). Neuropeptides. 2011 Jun;45(3):189-95.