[This post was first published in the Fairfax NZ Sunday Star Times on 31 August 2014]
In last week’s column I advocated that the mainstream dairy industry should convert New Zealand herds away from the production of A1 beta-casein. To not do so creates unnecessary long term risk to the industry. However, the mainstream industry remains locked into a defensive position.
In this article I will therefore briefly review some of the major strands of health evidence. I cannot cover it all – it took me a whole book to do so back in 2007. Since then, there has been a lot more evidence forthcoming.
In assessing the evidence, it is helpful to recognise that A1 beta-casein is the consequence of a historical mutation. Goats, sheep camels, buffalo, Asian cattle and humans produce beta-casein that is totally of the A2 type. It is only cows of European ancestry which produce A1 beta-casein.
In modern dairy herds, the proportion of A1 beta-casein varies by country, by breed and by herd. In New Zealand, there has been a slow drift towards A2. About 40 percent of New Zealand cows now produce beta-casein that is all A2, and most of the rest produce a 1:1 ratio of A1 and A2 beta-casein. A few animals produce only A1 beta-casein.
None of this would matter if it were not that A1 beta-casein on digestion releases a peptide (a protein fragment) called beta -casomorphin-7 (BCM7), whereas this does not occur with A2 beta-casein. Even the European Food Safety Report in 2009 conceded that this is correct. There is also no doubt that this peptide has opioid characteristics. It is a well-established scientific fact.
However, what has remained controversial until recently has been whether or not the BCM7 can pass through into the blood. Russian researchers have now shown quite clearly that it does pass into the blood of babies fed infant formula. They have also shown that a proportion of these babies are unable to metabolise the BCM7 efficiently between feeds and these particular babies have delayed psycho-motor (brain-to-muscle) development.
Russian workers have also found BCM7 in the urine of all children on normal milk diets. Polish researchers have even found that mothers who are themselves drinking cow milk can pass bovine BCM7 to their babies in breast milk.
The original evidence implicating A1 beta-casein came from Professor Bob Elliott from Auckland University. He noted that Samoan children brought up in Samoa had a minimal level of Type 1 diabetes whereas children of Samoan ethnicity in New Zealand are vulnerable. He looked for differences in lifestyle, and identified exposure to cow milk as a possibility. Subsequently working with Dr Murray Laugesen, he showed that across the developed world more than 80% of the between-country variations in Type 1 diabetes could be explained by per capita intake of A1 beta-casein. Corran McLachlan showed similar correlations between intake of A1 beta-casein and heart disease. The correlations are statistically very strong and no alternative explanation for these between-country differences has stood the test of time.
A human clinical trial from Curtin University in Australia, recently published in the European Journal of Clinical Nutrition, found that there were statistically significant differences in digestive symptoms between milks containing A1 and A2 beta-casein. This has drawn attention back to some of the animal trials for explanations. For example, a New Zealand trial with rats, undertaken by AgResearch and co-funded by the New Zealand Government and The a2 Milk Company, and published earlier this year, found increased levels of an inflammation marker MPO in the colon on the A1 diet. I am a co-author on both the Curtin and AgResearch papers.
A similar study with mice, published last year in the European Journal of Nutrition, found comparable inflammation results. That study also found strong immunological responses to the A1, with greatly increased levels of antibody production.
The New Zealand ‘AgRats’ study also found, as expected, that the opioid effects of BCM7 from A1 beta-casein slowed down the passage of food through the rat intestines. Intriguingly, the A1 beta-casein also significantly increased the release of an enzyme called DPP4. The reason this is so intriguing is that the modern gliptin drugs, now widely used to control Type 2 diabetes, act by inhibiting this enzyme, whereas with A1 beta-casein the level increased.
There is a lot more research of relevance, including arterial plaque in rabbits and increased antibodies to oxidised LDL in humans. I now have several hundred published studies of relevance in my database. There is also a stream of additional studies in the pipeline about which I am very excited. There is no chance this issue will go away.
Next week, in the last of this series on A1 beta-casein, I will explain how to eliminate production of A1 beta-casein through breeding. I will also look again at the industry politics of A1 beta-casein and why the industry is so defensive.