30 JANUARY 2008 ISSUE
A1 and A2 milk: what is the fuss?
Keith Woodford is professor of farm management and agribusiness at Lincoln University. His book Devil in the Milk, published last year by Craig Potton Publishing, caused a stir with its reports of the detrimental effects of A1 milk. Professor Woodford tells his story.
A1 versus A2 milk has been a media “fringe” story for much of this decade. The publication of Devil in the Milk and reports from the New Zealand Food Safety Authority last year placed it in the spotlight. The key question is whether this is just a beat-up, or are there really major public health issues relating to type 1 diabetes, heart disease, symptoms of autism, and general milk intolerance? The way to answer this question is to go back to the science and look at the evidence.
The A2 story started in 1993 when Professor Bob Elliott from Auckland asked whether there was a difference between the milk the Masai people of Kenya drink and the milk drunk in Western countries.
Professor Elliott already knew casein was diabetogenic in rodents. He also knew Samoan children in New Zealand had 10 times the incidence of type 1 diabetes than Samoan children in Samoa.
And he also knew the Masai people of Kenya, who drink very large amounts of milk, do not get type 1 diabetes. So, he rang the Dairy Research Institute, asked to speak to a milk biochemist, and then asked whether there were any differences between the Kenyan milk and our own. The answer was that there is a difference in the beta-casein.
The non-disputed facts are a mutation, occurring some thousands of years ago and affecting the forebears of modern European cattle, has meant many European cattle produce a variant of beta-casein that has the amino acid histidine in position 67 instead of proline. As a consequence, the peptide beta-casomorphin7 (BCM7, which I also call the “milk devil”) is released on digestion.
There is no dispute this is a strong opioid. It takes about 10 times as much naloxone to counteract a molecule of BCM7 than is needed to counteract morphine. Rats injected with BCM7 show bizarre behaviour patterns within one minute of administration, and there is clear evidence this peptide crosses the blood/brain barrier with ease. It then attaches to the mu opioid receptors. Fortunately, in most people this peptide cannot cross from the intestine to the circulatory system. But there are some people, who for any of a range of reasons have a permeable intestine, for whom this can occur.
Professor Elliott looked for evidence in two ways. One was to feed some non-obese diabetic (NOD) mice A1 beta-casein and feed the rest A2 beta-casein. None of the mice fed A2 became diabetic but 47 per cent of those fed A1 became diabetic. Administration of naloxone prevented another group of mice fed A1 from becoming diabetic.
Professor Elliott and colleagues also looked at the human epidemiology.
The most informative paper is Laugesen and Elliott’s 2003 paper in the New Zealand Medical Journal, “Ischaemic heart disease, type 1 diabetes, and cow milk A1 beta-casein” (NZMJ 2003 24;116[1168]:U295). This paper reported extremely high correlations at the country level between A1 beta-casein intake and type 1 diabetes (see graph). Statistically, the chance of this being caused by fluke data associations is much less than one in 1000. Subsequently, it has been shown that type 1 diabetics have considerably higher antibodies to casein than non diabetics, and that it is specifically A1 beta-casein antibodies that set them apart. A highly plausible explanation for the autoimmune response is that the same sequence of four amino acids occurs at the end of the BCM7 molecule and in the GLUT2 insulin transporter molecule produced in the pancreatic islet cells.
And there is also strong evidence from Finland that high intake of ordinary milk is a major risk factor for diabetes.
The commonly cited counter evidence to all of the above is a multi-country trial with rats and mice where Professor Elliott’s earlier findings were only weakly confirmed. (Beales et al. A multi-centre, blinded international trial of the effect of A1 and A2 beta casein variants on diabetes incidence in two rodent models of spontaneous Type 1 diabetes. Diabetologia 2002;45:1240–1246).
However, what has never been publicly disclosed is that the NZ Dairy Research Institute, which supplied the diets, knew before publication of the paper in Diabetologia that the A2 diets had been heavily contaminated with BCM7. This BCM7 had been identified right from the trial as the putative cause. I set out the documentation around this issue in my book. It is a huge issue of scientific ethics.
The evidence in regard to heart disease came initially from Corran McLachlan. In 1994 he was reviewing work by Professor Elliott and was astonished to realise the between-country incidence levels of type 1 diabetes and heart disease were highly correlated. Remarkably no one had recognised this previously. On further analysis he also found extremely high correlations between heart disease and A1 beta-casein.
Subsequently, Julie Campbell from the University of Queensland led a team that fed A1 versus A2 beta-casein to rabbits. The A1 rabbits developed arterial plaque and the paper (A casein variant in cow’s milk is atherogenic. Atherosclerosis 2003;170[1]:13–9) concluded A1 beta-casein was atherogenic. Other scientists from France have found BCM7 oxidises LDL. Scientists from the Czech Republic have found babies fed ordinary cows’ milk (which contains the A1 beta-casein) have much higher levels of antibodies to oxidised LDL than is the case with those who are breastfed. Of relevance here is that breast milk is of the A2 type.
The scientific evidence for autism symptoms comes primarily from three groups of workers in the US, Norway and the UK. This is linked to the well known fact many autistic children have intestinal issues and associated gut permeability. They have shown that autistic children typically (but not always) excrete BCM7 in their urine. This can only come from milk. When milk is removed from the diet the autistic symptoms decline and the excretion of BCM stops. The major criticism of this work has been the lack of blinding of the subjects of the trials. However, there is evidence from trials where the investigators were blinded. There is also a great deal of anecdotal evidence. As one New Zealand mother, who has been using A2 milk for several years said to me just recently: “the cognitive is more exciting, he is simply not ‘zoney’ like he used to be.”
The evidence in relation to milk intolerance is largely anecdotal. However, there are undoubtedly a considerable number of people who have previously considered themselves lactose intolerant who are now finding they can tolerate A2 milk. The inference is their intolerance was in fact to A1 beta-casein. And another example from the mail bag: “My sister drinks only A2 milk, she has IBS. She finds it a godsend and calls it ‘her milk’.”
In relation to the age-old story milk stimulates mucus and phlegm, it has recently been shown BCM7 stimulates the production of mucins, which are the proteins that makes mucus thick and sticky.
There is of course a lot more evidence, and in my book I draw on over 100 peer reviewed papers.
The NZFSA continues to argue there is no risk difference between A1 and A2 milk. Until recently it has based this on its interpretation of Boyd Swinburn’s 2004 report on this issue – Beta casein A1 and A2 in Milk and Human Health. But Professor Swinburn has made it plain in correspondence to NZFSA, which I obtained through the Official Information Act, that he considered their interpretation to be “spin”.
NZFSA argued my book is not scientific (then admitted not having read it).
The solution seems obvious. We already have more than 1 million pure A2 cows and we could breed the rest across within two cow generations (about 10 years). In the meantime, we could put the A2 milk into priority products such as drinking milk, infant formula and ice cream. These are products from which we believe the release of BCM7 can be high. A1 could be used for products such as cheese, butter and whey powders, for which the A1/A2 status is much less important. There would be some logistical issues, but the major barrier to progress is industry politics and intransigence. Entrenched interests, including non-disclosed associations between researchers and industry are just one part of this.
There is already A2 milk available in many New Zealand cities (and labelled accordingly) but wider availability is needed urgently.
Copies of the Boyd Swinburn report, Beta casein A1 and A2 in Milk and Human Health and the lay summary can be found under ‘Reports’ on www.nzdoctor.co.nz
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"Two reviews planned for A1/A2 milk debate"
Media release from food safety minister Lianne Dalziel (13 December 2007)
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