Take the Green’s Candidate Test

It is good to see Frog is appreciating my efforts to highlight their candidates and candidate selection process. I do actually think it is not a bad idea to have some sort of test to see how well candidates do when confronted with an issue, and asked to formulate some lines.

Now in case the need some more candidates, I thought I’d give people here the opportunity to enter their own responses. Today we will start with the A1 vs A2 milk issue.

The background story the candidates were given is after the break. Go read it and then complete the following in the comments below:

After reading the ‘A1 or A2’ article:

1. Pick out the main points, and summarise as three bullet points (one sentence each; the length of that sentence is up to you!) Time guide: 15mins, including reading the article.

2. As you cross the lobby of Parliament on the way to the House, a reporter from Radio New Zealand approaches you and asks for comment on the A1/A2 milk controversy.  You need to come up with a couple of “soundbites” which succinctly and compellingly give the Green perspective.  Time guide: 10 mins.
 

A1 or A2 milk? Where’s the research?

The following is a summary of New Zealand government-sponsored research, clinical or otherwise, into A1 and A2 milk since July 2004:  None.

Why July 2004? That was when Professor Boyd Swinburn, public health specialist at Deakin University in Melbourne, published a review into existing research on A1 milk and human health risks such as diabetes and heart disease.

Swinburn’s study, for the New Zealand Food Safety Authority, said the need for further research was “abundantly clear”. Because of vested commercial interests, he said, “the appropriate government agencies have several important responsibilities in this matter: to support further research in the area (especially clinical research); to clearly communicate the state of knowledge and judged risks to the public; and to take specific actions to promote and protect the health of the public. “The first two actions are clearly warranted based on the evidence to date.”

Most of the milk we drink contains A1 beta-casein, a kind of protein commonly produced by the Friesian cattle breed. The other kind, A2 beta-casein, is more common in Jersey cows, for example. Goats’ milk is all A2, as is milk from native Asian cows. One theory, supported by several research studies but by no means proven, is that A1 milk increases the risk of diabetes and heart disease. Swinburn’s advice that more work was needed seems unequivocal, yet none was done.

The Health Research Council, which manages government investment in public good health research, has funded no studies relating to A1 and A2 milk, ever.  Auckland diabetes specialist Professor Bob Elliott sought Health Ministry approval to fund a repeat of a potentially important animal study, which was later found to be fatally flawed by contaminated feed supplied by the NZ Dairy Research Institute.

The ministry declined to meet the several hundred thousand dollar cost of the project. The ministry has since approved no further studies and cites the Food Safety Authority as the relevant body, although the FSA has also neither promoted nor funded any scientific follow-up to Swinburn’s report.

Food Safety Minister Lianne Dalziel told the Sunday Star-Times on Thursday: “NZFSA has no mandate or facility to sponsor clinical research itself, which is why no further research was undertaken despite the recommendation in the Swinburn report. “When I was briefed on the A1/A2 milk issue late last year, I felt this was a gap in the process. I believe that any such recommendation should be assessed by health or science and research officials and a decision made about whether further action is required.”

Two weeks ago, Dalziel announced a further review of existing scientific studies. This will be done by the European Food Safety Authority after inquiries by New Zealand officials discovered it was also interested in the subject, which neatly flicks the burden of responsibility and funding on to the Europeans.

Dr Murray Laugesen, a public health scientist and co-author of research relating to A1 and A2 milk in 2003, said Dalziel’s announcement would achieve little. “OK, so they do another review of the existing evidence that won’t get you anywhere at all. It’s like washing the same clothes twice. The main purpose seems to be to get the NZFSA off the hook, to get clarity where clarity is not possible.”

The EFSA’s conclusions are not expected before the end of this year, but already their value is in doubt. In a January letter to EFSA head Catherine Geslain-Laneelle in Parma, Italy, her New Zealand counterpart Andrew McKenzie advised her to note the Health Ministry’s view that “further research, especially independent human trials and animal experimental studies, will be required to definitively identify A1 beta-casein in milk as a risk factor in disease”.

Whether the EFSA will come up with definitive results from its review is unclear since so little science has been done in the interim. But if Geslain-Laneelle, an experienced bureaucrat who speaks three languages, needed guidance, McKenzie advised she read Devil in the Milk, a review of A1/A2 science by Lincoln University professor Keith Woodford. It was good advice. Woodford’s book, published in September, awakened the sleeping giant of controversy over A2 milk with a collection of evidence from more than 100 research papers (Swinburn had reviewed 38).

The issue goes back to the early 1990s, when Elliott got together with dairy industry scientist Dr Jeremy Hill to examine potential links between milk consumption and Type 1 diabetes. Their hypothesis was that the culprit could be in the beta-casein proteins found in milk. Elliott and Hill’s study of international data, funded by Fonterra predecessor the New Zealand Dairy Board, found that the incidence of diabetes and heart disease was correlated with consumption of A1 milk. The correlation is acknowledged by scientists of all stripes to be unusually strong but it does nothing to prove that A1 milk actually causes these health problems.

The latter point is what several scientists have been working on ever since. The evidence to date, as presented by Woodford, suggests it’s worth persevering with the effort.

Fonterra did enough work in this area to own important patents around A2 milk and related genetics. The other main owner of patent rights is New Zealand‘s A2 Corporation, which acquired them from the Child Health Research Foundation a funder of Elliott’s research. However, Hill and Fonterra have since become sceptical of the A2 hypothesis and the giant co-op no longer funds research exploring it.

The dairy industry’s position is understandably awkward. If its research found evidence of links between A1 milk and disease, it would be faced with marketing a compromised product while simultaneously promoting its alternative, A2. Then there is the thorny question of legal risk. If A1 was subsequently shown to be a factor in diabetes, for example, and Fonterra had known about it, the potential costs of legal action would be truly eye-watering. Furthermore, any general loss of confidence in milk as a source of nutrition could have a significant financial impact on dairy companies and by extension on New Zealand. Fonterra is so big and so important to this country’s economy that the repercussions would be felt far and wide. So its position is naturally one of careful risk management note the science is inconclusive, monitor developments but do nothing to promote further research.

A comment from Fonterra CEO Andrew Ferrier exemplifies this view: “Whenever any new science (both good and bad) about milk and its components is presented we carefully review that science. We have done this on a number of occasions on this issue and found no cause for concern.”

Behind the scenes, however, dairy farmers may be heeding Swinburn’s advice to consider changing the composition of their herds. Thanks to the industry’s work, it is now a relatively simple matter to classify cattle according to A1 and A2 genes. As Swinburn noted, “a New Zealand dairy herd that produced predominantly A2 milk would have no apparent negative health effects and could potentially have significant population benefits if the A1/A2 hypothesis proved to be correct”.

According to cattle genetics specialist LIC, about one million of New Zealand‘s 3.9 million cows are now A2. The farmer-owned company does not have a view on whether A1 or A2 traits are desirable but said in its spring newsletter that it could respond to market demand for A2 semen within 48 hours.

When the Star-Times spoke to LIC in September its view was that there was sufficient genetic variation within A2 bulls to avoid losing other desirable traits. The New Zealand herd could be almost entirely A2 in eight to 10 years, it said, and the shift “could be done without compromising other genetic qualities”.

Last week LIC’s general manager of genetics, Peter Gatley, said the picture was not quite so simple. “There is always a trade-off,” he said. “Any time you require a certain trait you have to let go other genes. “As we restrict the total gene pool to the third [with A2] you immediately diminish the gene pool. A large diverse gene pool is always a good thing and to make any move to restrict the gene pool is a major step.”

So although the move could be made, there is a good reason not to do it if the benefits are uncertain. In terms of New Zealand‘s fresh milk supply, milk from one million A2 cows is more than enough to meet local needs if there was any demand for it. Collecting it would require some reorganisation, however, because the animals tend not to be gathered into complete herds.

This country’s biggest marketer of A2 milk, Hamilton-based Ridge Natural Foods, has two of its own A2 herds and milks about 180 cows year round. One other local farm supplies Ridge but the company says it needs more. There are several other herds wholly or nearly 100% A2, but their milk is supplied into Fonterra’s pool and not separately marketed.  The question, then, is not whether anything can be done if A1 milk turned out to be a problem there is a clear path towards a solution. The question is whether there is a problem. 

 A1, A2: THE DIFFERENCE

– About 80% of the protein in milk is casein, which combines with calcium and phosphate to form molecules giving milk its opaque, white appearance.
– About 35% of the casein is beta-casein, which has three main genetic variants known as A1, A2 and B.
– A2 beta-casein differs from the others in that when digested it does not lead to the release of an amino acid in the body called beta-casomorphin 7 (BCM7).
– BCM7 is known to be an opioid – a type of narcotic – which can have a variety of effects, including suppressing the immune system. Some scientists suspect that BCM7 could cause or aggravate a range of health problems in susceptible people, such as diabetes, coronary heart disease, and autism. Research has found evidence to support these theories, but not enough to be conclusive.
– Milk can be tested to identify A1 or A2 beta-casein, and cattle can be tested to identify whether they carry A1 or A2 genes, or both. Milk in western countries, particularly milk from Friesian cows, tends to be A1.

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