Teasing out the beta-casein evidence

[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.

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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. Bookmark the permalink.

12 Responses to Teasing out the beta-casein evidence

  1. Honora says:

    Looking forward to more on this from you. It might answer the questions I had on your previous post. Thanks.

  2. Pingback: Rural round-up | Homepaddock

  3. Happy to hear you are publishing on this. As a non-New Zealander I looked up this paper and see it has a circulation of over half a million, which means it should reach a significant fraction of those in NZ that need to be reached.

    It appears from the data in the article that NZ cows produce appreciably less a1 milk than those in other western countries (the US, Canada, and Europe). It seems to follow logically that NZ milk and NZ casein containing products should be healthier than almost any others on the local market. A2 brand milk is rare or completely unavailable in these areas. While by looking for milk from certain breeds, notably Guersey’s one might do even better, the opportunity to buy milk from certain breeds is rare.

    The conclusion is that when these results get publicity in the West, milk sales may drop, but the NZ products should have an advantage. This could be especially important in baby formula and ingredients for it.

    The A2 patents in the US and Europe are near expiration, but their existence could slow down competition in these countries.

    Last time I looked the only semen seller in the US which provided the a1 status of their semen was the NZ one (I believe the patents had made US sellers unwilling to provide this information).

    When I talked the the US Department of Agriculture branch that helped on the gene chip that was widely used in the US, there chip did not provide the key genetic test, and this was because of the policy of staying away from markers where intellectual property rights were claimed. Since then the US Supreme Court has declared genes are not patentable, so in theory the chips could make this information available to herd owners for breeding.

    However, currently NZ is ahead of most countries, and should be able to benefit in the short run to increase their share of the market.

  4. Hello Prof. Woodford! I am not sure if A1 vs A2 is the difference but I thought I will mention some data that may or may not help support your theory.
    I had no trouble and still have no trouble digesting milk in India where I grew up. Even during the last visit a few months ago, I thoroughly enjoyed milk and milk products with no problems.
    I have lived in the US for the last 25+ years and a decade or so ago, I started having severe problems digesting milk sold in US (which I believe is A1-dominant). Milk powder is the worst culprit. However, in US, I can take the local lactose-free milk without any problems. Clearly lactase is not the issue since I don’t have to take LF milk or lactase pills in India.
    I know of several (but not a large number) of fellow Indians who have had similar problems but with varying degrees of impact.

    • Keith Woodford says:

      DK, The most likely explanation is that you have a mild intolerance to lactose owing to an insufficiency of the lactase enzyme. Because of this insufficiency, some of the lactose is not metabolised and instead it ferments. This then becomes much worse in the presence of BCM-7 derived from the A1 beta-casein. This is because the BCM-7 will be slowing down the transit of food through the intestines, and this is giving increased chance for the lactose to ferment. Fermentation is an exponential relationship so it only takes a modest slowing of the transit of food for this to have a big effect.
      Keith

  5. Phred Linn says:

    Hi Keith,

    I really enjoyed your book and want to thank you for your efforts.

    I have long known my family does not tolerate cow milk well and have therefore been milking goats for years just for our table milk.

    I have recently done the 23 and Me genetic test and am fascinated by the ability of this test. I’m wondering whether anyone has tried to figure out what genes might be responsible for making the difference between being able to tolerate A1 milk or not.

    In the US all school age kids are given milk for dinner and essentially forced to drink it. It’s A1 skim milk. If you knew your child had this problem then you would be able to manage the issue much better.

    Thanks again

    • Keith Woodford says:

      Hello Phred
      We do not have that information.
      I think it will be multiple genes that affect susceptibility.
      The relevant genes will be the ones that affect auto immunity and also possibly gut permeability.
      Keith Woodford

  6. Ghulam Abdulla says:

    Hello professor Woodford, I’m amazed by what you have uncovered and am currently trying to spread awareness of your work amongst colleagues and health professionals.

    A quick question, if I may, my entire family have been shown to have high levels IgE antibodies in their blood having tested positive in a milk allergy test. My wife and children drink cows milk. I have interpreted these results to mean that they are reacting badly to the milk and need to change to Sheep’s, goats or buffalo milk, and in a potentially fermented form, for example, yogurt or kefir.

    Would you agree?

    My son has severe eczema. My wife has high blood pressure aged 35, I am now starting to think it is BCM7 related. She seems addicted to milk! So does my son!

    Thanks

    Ghulam

    • Keith Woodford says:

      Ghulam,
      I do not have the formal medical qualifications to give you specific advice.
      However, I do draw to your attention that allergies are not the same as intolerance,and milk allergies can be caused by milk proteins other than A1 beta-casein and its casomorphin derivatives(e.g. BCM7). So the same allergies could still occur with a2 milk, and hence caution is appropriate.
      With those provisos, and based on your information that your family do currently drink a lot of cows milk, and assuming you are in the UK as your email address would indicate, then you should be able to find a2 milk as an alternative which you could try. Alternatively, you could try sheep, goat or buffalo milk. It should not be necessary for these to be fermented products unless your family members also have an underlying lactose intolerance
      I think it is likely (but not certain) that you will see a positive effect for the eczema and hopefully this should be evident within a month. In regard to blood pressure, there could be other underlying causes requiring deeper medical investigation, but shifting away from cows milk containing A1 beta casein would be a good place to start. Your wife should be able to assess in a couple of weeks whether or not she feels in better health, but I would expect any blood pressure benefits to be long term rather than short term.
      Keith Woodford

  7. Keerthi Kumara says:

    I am Sri lankan & Veterinary surgeon, Our dairy breeding policy depend on cross breeding ( Local breed cows have been crossed with Jurcy & Frecian seaman Through AI ) . So we produce type a1 cows through AI , So our policy makers & breeding specilist do not consider your A1 issue, They destroyed our milk industry , what is your advise to correct it , I appreciate your work . Thank U Sir

    • Keith Woodford says:

      Keerthi
      Your local cattle (prior to crossbreeding) will be close to 100% A2. Indeed if they are purebred indicus cattle then they will be 100% A2. The Jersey and Friesian semen you have been using will probably be about 50% A1 and 50% A2 (this is approximate), so the first cross progeny will be about 50% A2A2 and 50% A1A2. The solution going forward is to only use bulls that are A2A2. To the extent that the semen is coming from international suppliers, then these suppliers know the A1/A2 status of their bulls. But they don’t supply that information unless specifically asked for it. The local agents in Sri Lanka may not themselves have this information, but they can get it from the international head office if they ask. For locally produced crossbred bulls, there is a need to set up a testing system. One of the universities would have the expertise to be able to do this.
      Keith W

  8. Keerthi Kumara says:

    Thank u Sir for your reply. I forwarded your advise to our experts . they want details of compeny (produce A2 line seaman ), sir, If u have any information Pl let us know .

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