A1 beta-casein a threat to dairy industry

[This post was first published in the Fairfax NZ Sunday Star Times on 24 August 2014]

Evidence that A1 beta-casein might be a human health issue has been available for more than 15 years. However, the mainstream dairy industry has always fought against the notion that it might be important.

Back in 2007, I wrote a book called ‘Devil in the Milk’ which brought together the evidence at that time. The mainstream industry and even some elements within the Government were not impressed. They made it clear that this was an issue which New Zealand did not need to air publicly. The industry, with considerable help from the Food Safety Authority, was largely successful in dousing the public concerns, leaving just a few little puffs of smoke to remind those who were watching carefully that the fire might not be totally out.

In Australia, events played out differently. In 2007, ‘A2 Corporation’, which in recent months has been rebadged as ‘The a2 Milk Company’, was successful in gaining a secure foothold in Australian supermarkets. Its ‘a2 milk’ – which is free of A1 beta-casein – is now found in all major Australian supermarkets. Apart from Coles and Woolworth’s home brands, it is the leading brand of milk across Australia. It sells for more than twice the price of the supermarket home brands.

Within the last year, The a2 Milk Company has also launched an infant formula, ‘a2 Platinum’. It is produced here in New Zealand by Synlait on contract to The a2 Milk Company, and is marketed in Australia, New Zealand and China. Within New Zealand, the promotion has been limited, but in Australia it is clearly getting lots of traction.

All of this is relevant to New Zealand for two reasons. The first is that The a2 Milk Company is a New Zealand company, listed on the NZ stock exchange, and one of New Zealand’s largest agri-food companies by market capitalisation.  Due to release its latest annual financial results on 28 August, I expect they will report substantial further progress in Australia, but perhaps not in other domains.

The second reason is that there is a flood of new research now being published in the international scientific and medical journals demonstrating the relevance of A1 beta-casein to human health. The underlying cause is that A1 beta-casein digests to release a peptide (a protein fragment) which has opioid characteristics. The peptide is called beta-casomorphin-7, or BCM7. This translates as ‘a morphine-like fragment from beta-casein containing seven amino acids’. The effects are multi-faceted and every month we are learning more.

The key research which is bringing the beta-casein issue back to public attention right now has come from Curtin University’s School of Public Health. This research has demonstrated in a human clinical trial that A1 and A2 beta-casein produce statistically significant differences in digestive symptoms. This has received huge media exposure in Australia but only limited exposure in New Zealand.

The Curtin paper is published in the high ranking European Journal of Clinical Nutrition. From Lincoln University, I have worked directly with the Curtin team on this trial, and I am one of the four authors.

Ironically, I think there are actually more important papers that have been forthcoming in the last few months, but they were with animals. With rats, mice and rabbits, and under strict ethical guidelines, we can do trials that include tissue dissection. Of course this is not possible with humans. However, it has been the human clinical trials that the Australian media has latched onto. This has the potential to now refocus attention on all of the other new research. There is further research in the pipeline, some of it close to publication.

I have always argued that for New Zealand the A1 versus A2 milk issue could be either a risk or an opportunity. Unfortunately, to a large extent we have squandered the opportunity – by ignoring rather than managing the risk – and now it is about to become a real risk.

The way to get rid of A1 beta-casein is to breed cows that produce only the A2 type of beta-casein. It is easy to breed out the A1, but it takes time. Sheep, goats, camels, buffalo and humans only produce beta-casein of the A2 type. The A1 type is only in cattle and has been caused by a historical mutation.

There is a lot more to be said about A1 beta-casein, including specifics of the health implications, and the associated industry politics.

The big message is that New Zealand should quickly get on with the task of breeding its dairy herds to be free of A1 beta-casein. Unfortunately, that will take at least ten years.

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About Keith Woodford

Keith Woodford is an independent consultant, based in New Zealand, who works internationally on agri-food systems and rural development projects. He holds honorary positions as Professor of Agri-Food Systems at Lincoln University, New Zealand, and as Senior Research Fellow at the Contemporary China Research Centre at Victoria University, Wellington.
This entry was posted in A1 and A2 milk, Agribusiness, Dairy, The Fairfax SST Articles and tagged . Bookmark the permalink.

8 Responses to A1 beta-casein a threat to dairy industry

  1. Gerard Besamusca says:

    Hi Keith,
    Amazing on many levels. Amazing how it was denied and buried. Amazing how it was not acted upon a decade ago (an opportunity partly missed, although I understand most semen used these days is A2 type), amazing how even officials tried to put this back, amazing the press and public at large have taken so long to start realising the impact of this. Amazing the shortsightedness of some who tried to deny the science or at least the concerns raised at the time.
    We owe a lot to you for bringing this out in the open again and against the negative impact information suppressors have generated, especially when your book was published. Some people should be ashamed.

    Thanks

    Gerard

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  3. Honora says:

    Keith, I wonder why the semen is predominantly A2. This would indicate to me that indeed Fonterra etc. are concerned despite their denials. I know the issue is political but I’d been keen to have it explained why if they’re ostensibly not concerned, they’ve focused on A2 dominating in semen. I recall hazily from your book that it was mentioned that in 2005 that approximately 65% of the semen herd was A2. I’ve been buying the Retro Organics brand from Southland which originates from Jersey cows so hopefully am getting A2 rather than A1. They are unable to verify what their milk is. I think this is to do with the A2 Milk company being the only ones who are allowed to tout A2 in NZ.

  4. Louise McConnnell says:

    Keith, we are so pleased that you continue to highlight the risks that having milk contaminated with A1. For other readers interest we took the initiative to only use A2A2 semen over our dairy herd from 2000 and have let natural attrition remove the A1 cows from the herd. To accelerate the change we also tested each crop of calves and sold off all the A1 contaminated ones. We still have three A1A2 cows left in the herd – one of the problems of having good producing teenager cows! So we are still going on this change over after 14 years.
    The latest catalogue from LIC still has two A1A1 HOlstein-Friesian bulls listed, 15 are A1A2 and 19 are A2A2 – this will mean that there will be a lot of A1 contaminated milk! The Jersey is a lot better with only 3 A1A2 and the other 14 all A2A2. The Kiwi Cross team are not so good – 3 are A1A1, 10 are A1A2 and 11 are A2A2.
    Any A1 contamination of milk is not acceptable for those people whose genetics mount an immune response against it so it is not likely that NZ milk products will cleaned up any time soon.
    We have family members who cannot drink A1 milk but who have no problems on A2 cows milk so we know first hand that there is a problem with A1 milk. It is a great shame that NZ farmers have not had good advice about the up and coming costs that are going to come home to roost on this issue.
    We also run a small Red Devon stud and after doing some screening testing found to our horror the presence of A1. We have also had to raise A2 bulls to clean up the genetics here too. Why? Well not many Red Devon cows are milked although they were once a dual breed but there is some Australian work associating meat tenderness with A2A2. Also we have noted over the years of home butchered meat that Jersey (mostly A2A2) cross meat is often very tender. When an animal has the A1 gene present that means every cell in the body of that animal has A1 present and we are not aware of issues of A1 content of meat yet but then again is anyone looking?
    So sad to see that the NZ dairy industry hasn’t seen this issue as a huge opportunity.

    • Keith Woodford says:

      Louise, These figures for the LIC bulls (and indeed all of your comments) are very interesting. I used to watch these data closely, but with pressure of other commitments I have not been watching it lately. Is this for the Premium Sires team or is this for all the catalogued bulls? Assuming each of these bulls is used to the same extent (which will not be totally correct), then the A2 allele frequency in the sperm for the three breeds would be Holstein-Friesian 74%, Jersey 91% and Kiwi Cross 67%. This is still probably a slightly higher A2 allele frequency than in the NZ cow herd, which I expect is somewhere in the mid to high 60s. Readers from other countries should not assume that these allele frequencies apply in their own country.
      Keith

  5. Cliff Maurer says:

    I am curious about an apparent difference between A1 and A2 milk apart from the beta-casein. Some members of my family have a condition associated with deficiency of a lipase-related protein (LRP2). The effect of the deficiency is a reduced capacity to digest a pair of short chain triglycerides found in bovine milk fat.
    The problem is unrelated to lactose intolerance and is readily managed by using skim milk and avoiding butter in the diet. The condition is not particularly serious, except that it is apparently associated with a “fail to thrive” syndrome in infants which can be mistaken for a consequence of lactose intolerance.
    Quite by accident however, the affected members of our family have found that they can tolerate A2 milk and even A2 thickened cream products available in Australia without suffering the unpleasant (and embarrassing) problems which normally follow consumption of dairy fat.

    • Keith Woodford says:

      Cliff,
      This is the first time I have heard of this. What follows is my hypothesis as to what might be happening.
      We know that the BCM-7 which is released from A1 beta-casein slows down the passage of food through the digestive system. This is well proven in animals, and almost certainly is also the case in humans because the peristaltic movement of food is controlled by mu opioid receptors, and the BCM-7 attaches to them, messing things up. As well as that, we are seeing increasing evidence that BCM-7 has what we call pro-inflammatory effects in the digestive system. We have conclusive proof of this in animals, and supporting evidence in humans, but for obvious reasons getting the data from humans is more complex as we are not allowed to cut them up!
      So the likelihood is that the pro-inflammatory effects are worsening the deficiency of lipase related protein, and then the slower passage of food exacerbates the fermentation or whatever is happening to the undigested triglycerides.
      Thank you for sharing your situation with me.
      Keith W

    • Keith Woodford says:

      Cliff,
      A nutritionist colleague has pointed out to me that I was more than a little careless with one of my terms. I implied that the slower passage might be affecting the fermentation process..Clearly that cannot be correct in regard to fats, as it is only carbohydrates that ferment.

      My colleague thinks that a contributory factor could be ” methylation changes at the gene level coupled with proinflammatory effects, leading to extra short chain TGs in the system which cannot be absorbed and so will be ‘pooped out” . And as you will already know, more short chain triglycerides in the poo will create an urgent need to defecate.

      So the short answer is that we really don’t know the full explanation but we think your personal findings make a lot of sense.
      Keith

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