Updating ‘Devil in the Milk’

Since ‘Devil in the Milk’ was first published in September 2007, the story has moved on considerably. The purpose of this update (attached as a pdf) is to summarise the main events, recognising that it will continue to be an ongoing story, and only time will allow some events to be seen in their appropriate context. Essentially, there are three parts to the ongoing story. The first is about the politics of milk and health, how information is communicated, and market responses. The second is about what is happening ‘behind the scenes’ to Australian and New Zealand dairy herds. The third is about the new science. All are important to an overall understanding.
This update is meant primarily as an accompaniment to the NZ and Australian edition of the book. It is not a stand alone document. Some components of this update were incorporated in the American edition of ‘Devil in the Milk’, but aspects of the science update, in particular, are new since that edition.
devil update may2010


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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24 Responses to Updating ‘Devil in the Milk’

  1. Hello,

    Thank you for a very useful update.


  2. Adeha Feustel says:

    Hi Keith,
    Reading your book, I was continually thinking about vitamin D and sun exposure. What could the connection be? Interesting that the milk peptides are opioids similar to benzodiazepines, which are cleared by the glucuronidation liver detoxification pathway, which is the pathway involved with premature babies who have bilirubinemia. UV light, or just plain light, helps the body clear the bilirubin, either accelerating the pathway, or diverting the toxin, I’m not clear on how it works, just that it does. Maybe this is the vitamin D/sunlight/ latitude connection between the A1/A2 epidemiology. More sunlight clears the BCM7 via the glucuronidation pathway. (Riboflavin should also help.) Anyway, just a fun thought.


    • Keith Woodford says:

      Hello Adeha
      I am convinced that vitamin D is important for a range of health conditions. That includes a range of cancers. it includes osteoporosis and possibly prostate cancer.
      I think that winter exposure to sunlight is likely to be particularly important.

      In the case of Type 1 diabetes, I am sceptical of the latitude effect because the statistical explanation that it follows is modest, and there are lots of anomalies that have to be explained away for that hypothesis to be retained..
      Laugesen and Elliott did not, in their NZ Medical Journal paper, address sunlight per se. They only reported the latitide relationship. But Murray Laugesen has told me that they did investigate sunlight and it has no explanatory power at all in relation to between-country differences in incidence. There is some evidence that people who have Type 1 diabetes do have low levels of Vit D circulating in their blood.
      Whether the low VitD is a function of environmental or genetic factors is an interesting question.
      I cannot comment knowledgably about your specific hypothesis, but it does sound very plausible.

  3. Edward Miller says:

    I am puzzled that A2 Corporation has not yet succeeded in the US market, (at least to the limited extent it has in New Zealand and Australia). Not only is A2 branded milk not available on US stores, but even in the very specialized market for breeding cows and straws of semen it does not appear that they have had much impact, since one does not see the A1/A2 status of bulls advertised. Is this because they demanded too high terms, or have they made fundamental marketing mistakes, or simply not tried?

  4. Keith Woodford says:

    They have tried but with hindsight their strategy was flawed. But one should never underestimate the difficulty of bringing a new product such as A2 to market. It will be interesting to see whether they can replicate their Australian success across the world. Even in Australia they were initially less than successful, but are now making great progress. It’s worth having a look at their website at http://www.a2corporation.com where they have laid out the general direction that they intend to travel.

  5. Edward Miller says:

    Devil in the Milk leaves the impression that what can be called A1 and A2 milk should be identical except for histidine or proline at position 67.

    However, this does not appear to be correct.

    A2 Corporation has gotten US patent 7,851,147 issued December 14, 2010 (which refers to an earlier New Zealand patent 520016, filed Jul 03, 2002).

    In this patent they state that cows with a proline at position 67 (which we might call A2 cows) are expected to have a lower level of saturated fatty acid relative to unsaturated fatty acids. They also claim that such cows will have a lower level of short and medium chain fatty acids. The patent states that till recently it was believed that the fat content of cow milk and the beta casein type were unrelated. They state they have found an unexpected relationship (which is the scientific discovery which apparently underlies their “invention”), such that their A2 milk would be lower in saturated fat.

    Since saturated fatty acids are generally believed to increase heart attack risk, this could provide an additional benefit for drinking milk produced from A2 cows, such as A2 corporation is selling.

    From a marketing viewpoint it may be easier legally to advertise A2 milk as lower in saturated fat than other milks, since one is not saying that there is something bad in other milks (such as that it producing BCM7). I suspect they could use this finding to promote A2 milk (as a brand name) as heart healthier than other milks, since the saturated fatty acid heart disease relationship is well established. The application suggests their invention could be used to reduce the incidence of diseases associated with a high intake of saturated fatty acids including atherosclerosis, obesity, coronary heart disease, and diabetes.

    This patent does not disclose how their A2 cows differ from their A1 ones in omega 3 status. This would be an important question since high omega -3 is generally viewed as healthier. At least in the US, there are brands of milk that advertise being higher in omega-3 (done by feeding, not breeding, or selection of the cows). I hope the failure to reveal this is not because the effect is adverse, and something they do not wish to reveal. I would expect the research on the composition of fatty acids they did almost certainly included asking this very important question.

    From a scientific viewpoint this could somewhat confound the evidence that populations that drink more A2 type milk have lower coronary disease rates.

    A new (to me) fact is that BCM-7 seems to increase the intake of dietary fat in rats. This could provide a link to obesity. They say “Data from Lin et al. (1998, Peptides 19(2):325-31) suggest that .beta.-casomorphin-7 may modulate the intake of dietary fat.” Devil in the Milk (where what little I know about BCM7 was learned) lacks an entry for obesity, so that may be why it was news to me.

    Here is the summary of the patent (which can be found on the US Patent Office web site.
    Morris , et al. December 14, 2010
    Method of determining fatty acid composition of milk
    A method of reducing the level of saturated fatty acids relative to the level of unsaturated fatty acids in milk. In particular, the genotyping and/or phenotyping of bovine cows on the basis of the amino acid residue located at position 67 of beta-casein produced in their milk. The invention is based on the finding that there is a correlation between the ratio of saturated to unsaturated fatty acids in milk and the beta-casein variants in milk.
    Inventors: Morris; Christopher Anthony (Hamilton, NZ), Tate; Michael Lewis (Dunedin, NZ)
    Assignee: A2 Corporation Limited (Auckland, NZ)
    Appl. No.: 10/519,624
    Filed: July 3, 2003
    PCT Filed: July 03, 2003
    PCT No.: PCT/NZ03/00140
    371(c)(1),(2),(4) Date: August 15, 2005
    PCT Pub. No.: WO2004/004450
    PCT Pub. Date: January 15, 2004
    Foreign Application Priority Data

    Jul 03, 2002 [NZ] 520016

    • Keith Woodford says:

      I have not seen the scientific evidence to support these claims.
      Commerical firms often try to protect their patch by making patent claims at an early stage when the evidence is still incomplete.
      So I am cautious about making such claims.
      It is possible that if the gene determining A1/A2 status is on the same chromosome and close to a gene that influences fatty acid status, then one could act as a marker for the other. But personally, I want to see stronger evidence before I would make such a claim in ‘The Devil’.

  6. Edward Miller says:

    It is agreed that firms may apply for a patent early in order to protect their rights, and possibly before the evidence that something works is as solid as we might want. However, there can be advantages to applying late also, in that the late application gives a later date of expiration.

    On the face of it, this patent may be of little value since if you want to know something about fatty acids in certain milk, or the ability of certain cows to produce milk with desirable fatty acid content, you do direct tests of the milk, rather than drawing deductions from a genetic test for casein related genes. However, after A2’s others patents have expired, they will still be able to point to this patent to scare others away who may be thinking of producing milk that is low in BCM7, thus making their A2 brand more valuable.

    It does appear (from internet postings and a private communication) that worries about A2 Corporation legal action has prevented some from having their cattle tested, or from using the results of these tests.
    While the material in the patent are skimpy and some details are lacking, the sample size appears large and I find the results plausible. They claim to believe that the result is not due just to linked genes. In general, genes close to each other tend to be inherited together, and I would have presumed that selection for one things (say in the protein) might involve inadvertent selection for others. The Devil in the Milk claim that A1 and A2 milk would be identical in all ways except for BCM7 producing potential appears implausible on general genetic grounds.

    A purpose of the US patent system is not only to promote invention, but to lead to disclosure. The system here may have worked either to encourage A2 Corporation to conduct tests it otherwise would not have, or (more likely), to make available the results of tests that otherwise would otherwise be still sitting in a file drawer somewhere.

    As mentioned, one concern I have is that they may not disclose unfavorable information that also was learned such as exactly which unsaturated fatty acids increased. The absence of a claim about Omega 3 fatty acids makes me wonder whether they actually decreased, since they were almost certainly measured in the course of this study. There is one UK site (http://a2guernseymilk.com/cm/contact-info.html) which claims that Guernsey cows are not only very high on A2 beta casein but also much higher (three fold) in omega 3 fatty acid. They give no source for these claims and the omega 3 claims appears implausible to me (nor do I know anything about the owner of that site). I was surprised to see they used the brand name A2 on that site, which I would have expected A2 corporation to have objected to, since I am not aware of any licensee there.

    The other thing I learned from their patent was the reference to Lin et al article in Peptides on BCM7 and obesity. If calves produce BCM7 (do you know if they do?) there may be some benefit to a milk that breaks down in a way to encourage fat absorption. If so, it may help explain the spread of the mutation once it had occurred. It may also have led to the cow developing some mechanism such that if it carried the gene for BCM7 it produced a different type of fat for some reason.

    It was not immediately clear what the relevance of this work to their patent is. Mentioning it may be a way to make the effect they found sound more plausible. It may just be in there so that if so that if someone starts appears likely to bring out a non-BCM-7 milk and promoting it as reducing obesity, they have another excuse to threaten legal action over and possibly stop them.

    Do you know of any further work following up on that of Lin et al. (1998, Peptides 19(2):325-31) on BCM7 and fat absorption or obesity?

    • Keith Woodford says:

      I agree that selection for A2 could lead to selection for other traits, if the A2 allele is in effect a marker for an allele of an adjacent gene. Similarly, selection for specific milk traits could select either for or against A2. In NZ our herds have been drifting towards A2 for more than 10 years as a serendipitous consequence of a focus in our national selection criteria of efficient production of milk solids rather than yield per cow.
      I also agree that the A2 Corp patents are acting as a disincentive for some people to convert to A2 in North America and Europe. This is a frustration to me.
      I am not aware of any follow up work to that of Lin et al (1998).
      My current thinking is that the fatty acid patent is meant as a blocking patent to stop people circumventing other patents.

  7. Edward Miller says:

    Interaction of Glycation with the A2 type milk issue

    There is an interaction of the possible effects of glycation on BCM7 persistence in the body, mentioned in Robert Bartlett Elliott’s patent application (http://www.faqs.org/patents/app/20100130406#ixzz1PeA1iSAi) with the A2 type milk issue. Suppose heat treatment induced glycation does increase the harmful effects of BCM7. This would make the introduction of such milk especially important in countries where high temperature pasteurization is widely used. It would also suggest such plants should use A2 type milk.

    Since ultra pasteurized milk lasts longer it can be shipped greater distances, and this may make it possible for a firm to sell such a product over greater distances than for other milks. If people prefer such milk for some reason such as lack of refrigeration facilities, they might buy such a product if health conscious.

    Currently volume sales of milk from A2A2 cows seemed to be only by A2 Corporation. In the US there are seasonal swings in milk consumption which do not coincide with the spring flush in milk production. The solution is to use the surplus milk for easier to store products such as butter, cheese and powdered milk.

    I have often wondered what A2 Corporation franchisees do with excess milk when they have it. One story from Australia indicates a now defunct franchisee just dumped the milk. A farmer who had not been paid for his milk said he was surprised to hear they were dumping milk.

    One possible use for A2 excess milk might be to ultra-pasteurize it. Such milk might sold year round out of storage and supplied to those who either preferred it (for use on trips for instance) or who were too far from the factory to buy regular A2 milk.

    I understand that in New Zealand A2 only sells in the north half of the North Island (and a couple of other stores). Yet awareness of the issue apparently extends to the whole country. It might even be greater in the more rural areas (speculation) where the dairy industry is more important and issues related to milk are more discussed. It should be possible to place A2 ultra-pasteurized milk in at least a few stores in such areas where I would expect it to sell, even if in low quantities.

    An incentive for persuading some national authorities to encourage the production of A2 type milk (besides health benefits for their citizens) would be the possibility of expanding sales of their milk beyond their borders. Ultra pasteurized milk would be one way to do that over a larger area.

    Yogurt and Sour Milk Products

    If glycation of BCM-7 during pasteurization is a problem, reducing the amount of lactose (such as by fermentation) could reduce the amount of glycation and have health benefits.

    If the glycation primarily comes from galactose, just breaking the lactose down into galactose and glucose should not have an effect. According to Wikipedia: “Lactose-free milk can be produced by passing milk over lactase enzyme bound to an inert carrier; once the molecule is cleaved, there are no lactose ill-effects. Forms are available with reduced amounts of lactose (typically 30% of normal), and alternatively with nearly 0%. The only noticeable difference from regular milk is a slightly sweeter taste due to the generation of glucose by lactose cleavage. It does not however contain more glucose, and is nutritionally identical to regular milk.”

    If galactose can more easily glycated the beta casein or a precursor to BCM7 or BCM7 itself, this would actually make the milk less healthy.

    Reportedly galactose (half of lactose) produces glycation far more readily than glucose. “It appears that fructose and galactose have approximately ten times the glycation activity of glucose,” (Widipedia, citing McPherson JD, Shilton BH, Walton DJ (March 1988). “Role of fructose in glycation and cross-linking of proteins”. Biochemistry 27 (6): 1901–7. The abstract does not mention galactose, and this study is at lower temperatures, aimed at studying what might happen inside the human body.

    If what appears to be lactose intolerance is really a reaction to a byproduct of BCM7, such lactose free milk will not prove a solution, and the version in which the lactose is reduced by about 30%, might actually make the problem worse. A feasible test procedure for consumers might be to try lactose free milk and if that cannot be tolerated consider trying A2 type milk where that is available.

    the above leads to an obvious research project in which large numbers are tested this way.

    If it does turn out there are appreciable numbers who cannot handle lactose free milk but can hand A2 type, this could be a good marketing tool for A2 Corp.

    It would follow that fermented products such as yogurt might be safer, unless they were then sweetened by adding more sugar. If sweetened artificially they might be safer.

  8. Edward Miller says:

    Herd Segregation

    A probable reaction to suggestions that cows be segregated into different herds (such as could result from an effort to produce fluid milk unlikely to produce BCM7 when digested) is that merely moving the cows around will not change the total human exposure to BCM7. Yet, it would cost much money and result in higher operating costs for bottlers (as economies of scale went down).

    Of course, the first effect of companies like A2 is merely to move cows around.

    However, if A2 type milk brings a higher price, and milk surpluses are typically used for other products such as cheese, merely moving the animals around could improve health. Under US conditions, after moving the cows around, the human exposure to A1 beta casein would be reduced. More of the A1 milk would end up in cheese, and less of the A2 milk would end up in cheese (although I would hope some would end up in powdered products such as dried milk). Thus, a quick reduction in human exposure to BCM7 could be obtained by separating the cows, and then making cheese only from the milks with a high level of A1 beta casein.

    Dated (1994 information) at hand shows that in the US fluid milk sales are actually less than the sum of butter and cheese sales (in milk equivalents), so a major reduction in A1 beta casein in fluid milk could result merely from moving cows around and using different milks for different purposes. Such a reduction depend on the scientific question of whether choose really does produce much less BCM7 in human.

    In the US, a governmental program purchases cheese, butter, and dried milk to hold dairy prices up. Any reduction in consumer purchases of fluid milk, due possibly to concern about BCM7 in milk, is likely to result in increased government purchases and less of a reduction in dairy income than might at first be thought.
    (See http://www.idfa.org/files/Dairy7.pdf)

    Some reduction in dairy income would happen because fluid milk prices are higher than prices for the other uses.

    In such a market scenario, creating A2A2 herds would be in the interest of the industry, since this way the most health conscious consumers might be able to keep buying milk. If some farmer’s were forced out of the business, they might benefit if at least their A2A2 cows brought good prices (as they would).

    Such a sudden public concern could result in many A2A2 herds being set up. There could also be government programs that led to such herd segregation, including laws requiring minimum amounts of A2 beta casein in class A Milk (this is milk for human consumption), preferential purchasing of low A1 beta casein milk for military use or for school lunch programs, or taxes on high A1 beta casein milk. Such programs would likely result in much of the milk high in A1 beta casein being used for animal feeding (including calf feeding) and for cheese, butter, and dried milk (and probably industrial casein).

    O course, in such a scenario there would be a strong incentive to breed for cows able to produce A2 beta casein.

    The maximum benefit from cow segregation would occur if there were three type of herds, A2A2, A1A2, and A2A2, with the A1A1 always directed to cheese and casein for non-food uses (and for the “Sleepy Time” milk covered in Elliott’s patent), and the A2A2 preferentially to fluid milk (and certain powder products such as for baby formula).

    Such a threefold segregation could emerge if milk labels had to reveal A1 casein levels and there was enough public concern that low A1 beta casein products were desired, and bottlers paid farmers depending the levels of A1 beta casein. Those farmer’s who had mixed A1A1 and A1A2 herds (having already sold off their A2A2 cows) might find it profitable to sell off their A1A1 cows to reduce the levels of A1 beta casein in their milk. Others who produced for the cheese, butter, and whey markets might see an opportunity to acquire high producing cows at a good price.

    More likely, it could emerge by government action. In the US large quantities of cheese are acquired by a program intended to keep farm income up. This could be modified to pay higher prices for cheese from A1A1 herds, such that such herds were created by purchasing cows, removing the milk from the fluid market.

    Politically, this might be a way to reduce the loss of income for those farmers who happened to have heavily A1A1 herds.

    Hopefully, any such program would have a price that was too low to encourage actually breeding for the A1A1 type, or regulations would prevent it (such as requiring farmer’s in the program to use semen from A2A2 bulls), and limiting the benefits to cows alive or conceived prior to the start of the program.

    Milk segregation can also be achieved if the housing of the cows is in stalls (the stall or stanchion system) where they are milked and the pipes from different stalls go to different tanks. Some plumbing costs can be saved if all of the animals of one type are grouped together. This would involve selecting the cows on the basis of either genetic tests, or tests of the milk.

    There are several reasons for thinking specialized herds would be more economical. A2A2 milk is likely to be a premium price product, at least at first, and the sellers may wish to sell it also as “organic,” or coming from grass fed animals, or as having high omega 3 fatty acids. Maintaining these conditions are likely to affect the whole farm, so it seems best that all the animals on such a farm are A2A2.

    In the US milk is graded as Grade A or Grade B, with the Grade B used only for manufacturing. The sanitary standards are higher for Grade A milk and these regulations are most easily met if all of the milk on the farm is to qualify. I believe many of these rules are applied to the whole farm to prevent evasion by claiming milk was intended for manufacturing, and then slipping it into the Grade A tanks.

    Also fluid milk bottling plants and cheese or casein plants are often located in different areas. The bottling plants are often in or near large cities to minimize the costs of shipping packaged milk to the final consumers. The cheese, butter, and other plants are often in more rural areas closer to the milk supply. If this is the situation, moving the A1A1 cows to farms near where the cheese is to be produced, and A2A2 cows to near the bottling plants will minimize the total cost of trucking milk.

    A1A2 herds would logically be in intermediate locations where the destination of the milk might vary with time of year and market needs, going to bottling plants when more fluid milk is needed and otherwise to cheese plants.

  9. Sue Marriott says:

    Hmm.. I was interested to read in the updated postscript to D.in the M. (and many thanks for writing the book, btw) that heat treatment does not seem to alter the effect of BCM7. If the advent of pastuerisation of milk cannot be blamed for the increased effect of A1 milk in the last 150 years or so.. then what is it…. widespread use of antibiotics causing leaky gut? Multifactorial, I guess.

    I speak as someone who has ill effects from casein, gluten and high salicylates… following on from typhoid fever, cerebral malaria and prior to that mild food poisoning…. I’m guessing any one of which could be the ‘culprit’.
    For some 6 years I used raw milk which was a mix of Guernsey and Ayreshire.. and seemed to be fine until the last couple years, when I was obliged to change to Guernsey pasteurised. I also needed to cut out cheese (except sheep’s) and change butter over to Guernsey butter.
    How on earh is one to know, however, what other products these days, contain casein… widely used as a binder in processed foods, medicines, and as ‘technical casein’ in, e.g. nail polish!
    And just how much would such diverse casein containing elements in one’s life confound any ‘results’?!
    I’m now retesting the raw milk along with the use of charcoal as a possible antidote to those pesky number 7’s! We’ll see.

    • Keith Woodford says:

      Yes, I think it is multifactorial. One of those factors may well be that as general levels of hygiene have risen, and we no longer carry the parasite burdens of former times, that the body has become more sensitive to other ‘invaders’ such as BCM7. And I do know of some people who are sensitive to the casein that is used used as a binding agent in some (most?) muesli bars.

  10. Sue Marriott says:

    Yes.. it kinda makes sense to this non-scientist’s mind that the body (immune system) needs something to work on, as that is what it was ‘designed’ to do. But we don’t want to overburden the donkey! And I always get the feeling that when some wunderbar product is discovered as having beneficial application outside it’s original ‘remit’ that it becomes ubiquitous…. such is the folly of man. If we look at the natural world there is choice out there.. wide-ranging.
    Sue Marriott

  11. I have been vegetarian on and off through much of my life and over the last 9 months become largely vegan, prompted by Dr’s T.Colin Campbell (“The China Study”) and Caldwell Esselstyn (“Prevent & Reverse Heart Disease”) . They both are very down on milk generally for its implication in the onset of heart disease and cancer. They write more about casein . . . . Another more recent component of milk (and other animal products) I have been “looking up” is Nue5Gc. I have been trying to find what, if any, this may have to the work that you write about in Devil in the Milk and why mention of it does not appear in your book?
    Thanks for the opportunity to learn more from your blog

  12. Edward Miller says:

    Enzymes for Autism book dipeptyl dipeptidase IV

    An interesting book is Enzymes for Autism and Other Neurological Conditions by Karen DeFelice (2008), available from US Amazon for $14.59. enough of the pages can be read there to whet your interest.

    The general theory is that a leaky gut sometimes lead to autism. In addition to a special diet (such as casein/gluten free), or instead of them she report on experiences with using digestive enzymes to break down the problem peptides so they do not enter the blood stream. She and her sons were very sensitive to casein and found good results. For casein the idea of course is to add enzymes that break it down quickly enough so opioids do not enter the body.

    A key page is 100 where she discusses dipeptyl dipeptidase IV (DPP IV) and opioids.

    DPP IV prevent opioids from being absorbed by breaking the casein down earlier. This page and several others can be read on the Amazon web page for this book by searching for opioids or DPP IV. She mentions several commercial products containing it.

    This is partially an anecdotal book (many gathered from her internet discussion group), but with many scientific references included. She says in her case and that of her son, casein produced an immediate reaction within three hours. Her own first experiments were giving a ice cream sandwich plus enzymes, and fortunately observing no reaction. If there are many children like hers (and the book indicates there are), experiments would be relatively simple since it would not take a prolonged period of observation.
    This suggests a possible research strategy that would be relatively cheap. Locate autistic kids known to be sensitive to casein, and ideally ones showing BCM7 in the urine. Then see if their problems are reduced by using an enzyme product while drinking A1 containing milk. Also see if such problems are reduced by using A2 type milk. If the BCM7 and autism hypothesis is right, I would expect the kids responding to the two treatments to be the same (or at least show a high overlap).

    Ideally, the kids should be on a casein free diet originally, with ordinary milk (or ideally A1 milk) introduced as a challenge. The casein free diet as a starting point would be useful since there are others sources of casein than milk. I suggest A1 milk as the control both because there would be a greater effect, and because it is more standardized. Two ordinary milk samples may differ in the percentage of A1 beta casein in them.

    If experimenting with kids not on a special diet, A2 milk plus enzymes should also be tried.

    A benefit of enzymes over special diets (besides the greater convenience) is that it deals with the large number of ways casein got into the diet besides the obvious milk and milk products ways. Casein and milk solids are ingredients in so many foods that parents trying to feed a casein free diet (usually in the form of a case and gluten free diet) find it very hard.

    There would be obvious practical uses. If it works as far as the enzymes, many parents would have a useful tool. Obviously, if A2 milk could be drunk but not regular milk, there would be a powerful argument for drinking A2 milk and a powerful marketing tool for any firm that just might be producing A2 milk, possibly under the a2 brand name. Probably an optimal strategy for those with access to A2 milk might be using the milk, plus enzymes to deal with other sources of BCM7 producing caseins. There would then be a powerful argument for someone (Fonterra? or an Indian) bringing out a line of A1 beta casein free dried milk and other products.

    In the long run, even if they work, enzymes are probably not the best solution alone since they do cost extra, and not all parents will be willing to use them, Until their child is diagnosed, parents will not know to use them.

    It is possible that enzymes may have a long run use if there are other sources of problem peptides and children (or adults) whose bodies do not produce enough DDP IV to fully break them down.

    There are several product which are advertised as having DPP-IV. One is TriEnza with DPP IV Activity from Houston Nutraceuticals (and their web site shows several others), advertised on Amazon at $41.99 for 180 tablets (they suggest 2 before each meal). The book mentions other manufacturers with similar products. A quick web search shows still others.

    Enzymes for Autism and Other Neurological Conditions (Updated Third Edition) [Paperback]
    Karen DeFelice (Author)
    List Price: $19.99
    Price: $14.59 & eligible

    • Paperback: 384 pages
    • Publisher: Thundersnow Interactive; 3rd edition (April 1, 2008)
    • Language: English
    • ISBN-10: 0972591850
    • ISBN-13: 978-0972591850

  13. Keith, thank you for the update. In the four years since we last wrote, there has been useful activity. We now buy A2 (in Rangiora) consistently and are free of our previous digestive and mucous problems.
    As far as Fonterra is concerned, I admire their strategy. The economic consequences for N.Z. would be severe if (say) A1 were immediately outlawed. On the other hand, ‘permitting’ (or even covertly encouraging) A2 insemination would in due course provide the benign outcome with minimum social or financial disruption. I do know that some farmers deliberately seek A2/A2 sperm while others are merely happy to accept it. I understand that a ‘mixed’ herd using A2/A2 sperm will halve its A1 genetic proportion in each full breeding cycle. Even a ‘pure’ A1/A1 herd will be down to ‘only’ 1/8th A1 after four generations.
    If it were me, I’d do my best to deny any liability (for I would have got into that position by historical accident, after all) which means attempting to deny any effect, while at the same time maximising the rate of beneficial change – which would provide an excellent component of defense if it ever undeniably “all hit the fan”.
    All that is of course driven by the research, publication, and consistent debate that you and others continue to prosecute.
    Thank you again.

    • Keith Woodford says:

      Yes, you are correct. If a farmer uses A2A2 semen, and does nothing else, then the A1 beta casein content will halve with each cow generation. It takes 33 months from the insemination until the resultant calf enters the milking herd, but thereafter, the ‘halving’ of the A1 beta casein content will occur about every five years (assuming about 20% cow replacement rate). Speeding up the conversion requires genetic testing of animals, and linking this to cow culling and calf replacement. The prevalence of the A1 allele (variant) of the gene in the New Zealand herd has been drifting up in recent years and is now probably about 65%. But that is only an estimate based on my knowledge of the LIC bull team used for artificial insemination, as I have seen no recent tests on supermarket milk. In the United States it is probably about 50%. Some of the other key parameters also vary between countries. For example, in the USA, although the level of the A1 beta casein is currently higher, there tends to be higher cow replacement rates and hence a shorter cow generation.
      It is always good to hear reports of satisfied A2 consumers. The success of A2 milk in Australia, where it is in all Coles and Woolworths supermarkets (the two major chains) is largely a result of consumer ‘word of mouth’.

  14. Ian says:

    Are you aware of any evidence that links A1 milk consumption to the development of coeliac disease? There are all sorts of arguments about when to introduce gluten to children, yet the data doesn’t seem to be conclusive.

    The reason I ask is because Ireland *appears* to have a high consumption of A1 milk (at least from what I’ve read on betacasein.org) and a recent coeliac magazine stated that Ireland has one of the highest rates of coeliac disease in the world.

    Type 1 diabetes and coeliac disease can also occur together sometimes as well.

    Let me know if you are aware of any connection between coeliac disease and A1 milk.

    • Keith Woodford says:

      To the best of my knowledge, coeliac disease is unlikely to be caused by consumption of A1 milk. I think it is likely that the incidence of coeliac disease in Ireland is linked to a genetic pre-disposition. However, I think it is true that those who have coeliac disease are much more likely to develop a range of auto immune conditions, including Type 1 diabetes, than the general population. There are two reasons for this. The first is that untreated coeliac sufferers have a ‘leaky gut’ that allows peptides to pass through into the bloodstream. The second (and I am relying on recollection here and need to go back and re-read the literature) is that a key gene responsible for susceptibility to coeliac disease sits very close to other genes which influence leaky gut and auto immune conditions in general. From memory this is on either the fifth or sixth chromosome.
      So the practical significance of all of this is that conventional wisdom says it is OK for coeliac sufferers to consume milk, once gluten has been removed from the diet and the villi in the gut have repaired. But in my opinion it is sensible for these people to be consuming only A2 milk as they are particularly at risk of developing other auto immune conditions linked to the peptide beta casomorphin-7 that is released from A1 beta casein.

      • Sue Marriott says:

        That’s very interesting. And given (?) that antibiotics seem to be behind a lot of leaky gut cases (anecdotally), maybe in some distant future the indiscriminate use of antibiotics will be tempered by results of genetic testing! I wonder what alternative might they come up with!
        On a positive note, A2 milk has now become available in the shops in the UK. Hurrah… even if it is pasteurised and homogenised!

  15. C Hewton says:

    I use A2 milk as I cannot tolerate A1. I make my own yoghurt from this. Unfortunately this needs to be full-fat as there is no low-fat product available. I have seen a comment that the process of milk becoming yoghurt changes the A1 protein rendering it safe for the A1 intolerant to consume. Do you have a comment on this?

    • Keith Woodford says:

      I have only now seen your comment. The quick answer is that BCM7 will be released on digestion of yoghurt. However, if the right yoghurt bacteria from a live yoghurt culture manage to build up a population in your intestines, then it seems that they will gobble up the BCM7 that is produced. We still have more to learn about this. But personally I think it likely that consuming yoghurt – preferably A2 – is a good health strategy. I very much wish we had A2 yoghurt in New Zealand.
      Keith Woodford

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