Beta-Casein Paper in Journal of Integrative Medicine

I was recently invited to write a paper for the Journal of Integrative Medicine summarising the current state of evidence relating to A1 beta-casein, BCM7 and Human Health. The reference is:
Woodford, Keith 2011. ‘A1 beta-casein, BCM7 and human health’. Journal of Integrative Medicine. Vol 16(2):14-17.
A pdf is attached here.Woodford Jul 2011 Journal of Integrative Medicine

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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.
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8 Responses to Beta-Casein Paper in Journal of Integrative Medicine

  1. Edward Miller says:

    It is a shame that cheese does not seem to protect against the adverse effects of A1 beta casein. A report in the Journal of Dairy by A.S. Marziali and K.F. Ng-Kwai-Hang titled, “Science by Relationships Between Milk Protein Polymorphisms and Cheese Yielding Capacity” (Volume 69, Issue 5, Pages 1193-1201, May 1986) reports that cheese yields are higher for A1A1 beta casein milk than for A1A2 beta casein milk. This could be used to argue for segregating the A1A1 cows and using their milk for cheese and could provide political cover for removing such cows from the milk for bottling market.

    However, since there were only 3 A1A1 cows and 4 A1A2 cows, even though the results were statistically significant at the .01 level, I still feel the sample was inadequate in size.

  2. Ernest Worthing says:

    Hello Mr Woodford

    I was wondering if I may trouble you for direction to a post or document in which you react to EFSA report on the effect BCM 7? I am new to this topic and I’m trying to get multiple standpoints on the issue such that I may weigh up the facts. It seemed to me, on reading the EFSA report that they could find no notable correlation between the peptide and the effects you describe. Perhaps, in the light of little scientific consensus they were hesitant to commit to a verdict and instead concluded nothing? I am interested to know what you thought of their work

    Thanks

    Dr Worthing

    • Keith Woodford says:

      Dr Worthing
      I have not done a specific post on EFSA, but I have referred to it in the Epilogue to the updated version of ‘Devil in the Milk’. This update is posted on this site.
      I was less than impressed with the choice of the eight authors of the EFSA Report. By my analysis, seven of them have been closely aligned in either part or all of their careers with the dairy industry. There were no experts in the various health conditions linked to A1 beta casein. Within days of the release of the report, one of the authors was allegedly skiting at the Dairy Australia Conference that they had put the A2 milk issue to rest.
      Within the report there is some good science reported, and on occasions I do go back to this to refresh my memory on particular points. So some of the authors did do some good work. One useful finding was that under normal gut conditions BCM7 is indeed released from A1 beta-casein, but not from A2 beta-casein. However, from that point on they were more than a little selective as to how they used the evidence available to them.
      In efect. they knew the answer they wanted from the outset, and their terms of reference allowed them to come up with what they wanted. As Professor Swinburn commented at the time, their finding of no proof in relation to ’cause and ewffect’ was defensible but not helpful. One can always exclude all epidemiology using a criterion of cause and effect. If we used that criterion then we could claim there was still no proof that smoking causes cancer, and of course the tobacco industry did just that for many decades. One can also claim that animnal trials do not prove cause and effect in humans. But epidemiology and animal trials sure do provide lots of smoking guns.
      The findings of the EFSA report – or perhaps it should be called the lack of findings – depend very much on the argument that BCM7 supposedly gets broken down so quickly by DPP4 that even if it does travel from the gut to the blood then it will have no effect. Since the EFSA report, the Russian and Polish research on BCM7 in babies would seem to provide a strong counter to that perspective. However, because the research was undertaken in Eastern Europe rather than in Western Europe, or North America, or Australasia, this work has not yet got the traction that it deserves. And that in itself is a story. That situation will change once it is demonstrated from the so-called ‘West” that BCM7 is indeed to be found in the blood of babies and and/or adults. As to if and when that will occur, I remain impatient but I lose no sleep. The Russians and Poles may indeed have difficulty in getting traction in the English speaking world, but there is nothing wrong with their science.
      KeithW

  3. Dan Scollan says:

    Hi Dr. Woodford,
    I just listened online to a great 1hr interview you did. I have a few questions.
    Many times immune responses happen from a very small amount of protein, pathogen, etc..
    1. Does it only take a little A1 in susceptible individuals, like those with leaky gut, to have negative effects?
    2. Is milk that is 10% A1 less problematic for susceptible individuals, than say milk that is comprised of 30% A1? Is there a percentage threshold?
    3. You’ve said that a DNA test must be performed on a cow to determine whether or not that cow produces A2 – beta casein milk. I’ve heard that Guernsey and Jersey cows produce higher amounts of A2 than other American dairy cows. Is this true?
    Thank you for your time and keep up the great work!
    Sincerely,
    Dan Scollan
    Land O Lakes, FL

    • Keith Woodford says:

      Dan
      In terms of levels, less is better. With most of these health conditions, it is a case of probabilities, and the probabilities decrease as the A1 level decreases.
      There will be some people who are still susceptible at low levels, depending on genetic haplotype and extent of gut permeability etc. I know of one person who can identify the presence of A1 in milk (off the back of her tongue) when A1 makes up as litle as 2% of the beta-casein.
      Guernsey herds are typically about 90% A2 and some herds may be even higher.
      Jerseys are higher in A2 than Holsteins, but some herds can still be very high in A1, depending on the choice of herd bulls that has occurred. Also, in Jerseys, particularly it would seem in America, there is a proprtion that are neither A1 or A2 but B. This B variant is actually a derivative of A1 and there is some evidence that the second mutation affects what is called the tertiary structure of the protein, and that this leads to an even higher release of BCM7. So the simple message from this is that colour of the animal is a poor guide and genetic testing of DNA is necessary.
      KeithW

  4. Heather says:

    This B variant is not tested for in the A1A2 tests, so what genetic testing are you recommending?
    Thank you

    • Keith Woodford says:

      If not specifically tested for, then the B will show up as an A1. This is because they both have histidene at position 67, and hence both will release BCM7. There is some evidence that the B actually releases more BCM7 because of what is called the tertiary strructure of the B protein. What you can be sure of is that if you select for A2 then you will not accidentally be selecting for B; in other words, if B is not tested for specifically, it should never show up by accident as being an A2.

  5. J M says:

    Hi Keith,
    I enjoyed your book. I was wondering if there are any blood tests that test for the presence of BCM7 and is it only available to clinicians or those in academia? Entero Labs has a fecal test for sensitivity to casein but no blood test. It’s my understanding that most people who have healthy digestion have the enzymes such as DPPIV to break down BCM7 and can tolerate dairy but I am perplexed by people who can only tolerate A2 milk and not A1 milk. Some of these people have neurological or gastrointestinal disease which makes me think that in these individuals, it may be BCM7 (or a combination of BCM7 and gliadins as well as other toxins in the diet) that work synergistically to cause inflammation and wreak all sorts of havoc. Gluten and casein-free diets have been useful in treating neuro and GI diseases of late and it seems to me that BCM7 does indeed play a role in those cases. I am particularly concerned with raw milk because of anecdotes that claim that raw milk (especially if it is fermented) has helped those with autism, IBS, etc. and it makes sense because raw milk contains all the enzymes to digest the milk. And for those in which raw milk doesn’t help, it may be that they are getting raw milk but it’s from the wrong cows. Can you shed some more light on this issue? Thanks!
    Regards,
    JM

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