For more than 10 years, Alexandra Steinerova and colleagues from the Czech Republic have been untangling the causes of oxidative stress in infants. It is a fascinating story of how one investigation leads to another; of how BCM7 (beta-casomophin-7) and A1 beta-casein were subsequently implicated; and then how causation has been subsequently demonstrated.
The research is important because oxidative LDL (caused by oxidative stress) and antibodies thereto, are key risk factors and indicators of heart disease. They are also important indicators of Alzheimer’s disease.
Most people associate heart disease with easily measured cholesterol. But amongst researchers, oxidised LDL is much more important because it is this substance that makes arteries sticky and leads to formation of plaque.
The initial work of Steinerova and colleagues showed that, during the first few months of age, some babies have increasing antibodies to oxidised LDL, whereas others have declining values relative to levels at birth. In their first paper, in 1999, Steinerova and colleagues were unable to explain the findings.
Then in 2001, they reported that further work had shown that it was the babies on milk formula who had the increasing levels, and the breast-fed babies were the ones with declining levels. In fact, by three months of age the formula fed babies had almost 50 times the antibodies to oxidised LDL of the breast-fed babies. They offered no hypothesis as to which component(s) within milk formula might be causing this.
In 2004 Steinerova and her colleagues reported in the journal Atherosclerosis that they were by then hypothesising that it was caused by BCM7 from A1 beta casein. I mentioned this in my book ‘Devil in the Milk’ (published in New Zealand in 2007, with an American Edition published by Chelsea Green in 2009). But at that stage it seemed to me that it was still just a hypothesis, although supported by earlier work by French scientists Torreilles and Guerin who had shown in the test tube that BCM7 does indeed oxidise LDL. Accordingly, at that time I wrote: “this is an evolving story, with quite a lot known, but still much more to be discovered”.
Steinerova and colleagues published more evidence in 2006, but this was in a Czech medical journal (CS.Pediatria) and was not widely available to English-speaking people. It was only when Steinerova presented a paper in the United States at the XV International Symposium on Atherosclerosis in 2009 that the strength of her evidence became apparent. She now had new data not only confirming her original results (although this time the difference in oxidised LDL in formula-fed infants was only 18 times that in the breast-fed babies), but also now showing that the formula-fed babies had very high antibodies to BCM7 and A1 beta casein, whereas breast-fed did not. Equally important, the antibodies to A2 beta casein were much lower.
Arguably, there was still a weakness in the argument. These results were based on what is called epidemiology. This epidemiology clearly showed there was an association between A1 beta-casein and BCM7 on the one hand, and high levels of oxidative stress. And the statistical analysis showed that this was highly unlikely to be due to chance. But for those people who want proof rather than just exceptionally strong evidence, there was still no clinical trial. Where was the direct trial comparing A1 and A2 beta-casein?
In fact, Steinerova and colleagues do have an answer to that. In their 2006 paper in the journal CS.Pediatria they reported that piglets fed A1 beta casein had much higher and statistically significant levels of antibodies to oxidised LDL than did those fed A2 beta-casein. So yes, they have established what is known as ’cause and effect’.
So are there any remaining weaknesses in this line of work? Those who wish to deny the links between BCM7 and health (and there are plenty of those people associated with the international milk industry) will make three claims. The first is that the trial was with pigs and not with humans. That is true. But taking the combination of the human epidemiology and the animal results points only in one direction. The second criticism is that Steinerova has not published her recent work in top quality western journals, but instead she has published in a peer reviewed Czech language medical journal. Yes, that too is true. And until she does publish all of this work in English it will not receive the full attention that it deserves. The third criticism will probably be that the pigs when slaughtered at six months of age did not have visible heart disease. That too is true; but that is not surprising, for heart disease takes a long time to build up.
The bottom line is that Steinerova’s work provides chilling support to the prior body of heart disease evidence, undertaken by researchers such as McLachlan, Laugesen and Elliott, Briggs, and Campbell, which I report in my book ‘Devil in the Milk’. It also dovetails nicely with the new research from Natalya Kost and colleagues (see my post Russian breakthrough unravels BCM7 mysteries) showing that children fed formula not only absorb BCM7, but those who cannot then rapidly break it down or excrete it are likely to suffer developmental delay.
The bell is surely tolling. It tolls for those who continue to deny the evidence, and to those who fail to take the remedy of converting their dairy herds across to A2. Unfortunately it also tolls for those who as consumers are unwittingly exposing themselves to risk, but have little option in situations where A2 milk is not available.
This article originally appeared on Keith Woodford’s blog.