BCM7 and Sudden Infant Death Syndrome

Sudden infant death syndrome (SIDS) is every parent’s worst nightmare. In developed countries it is the biggest cause of death in apparently healthy babies. There are many strategies to reduce the incidence, including putting babies to sleep on their backs rather than on their tummies, not sleeping in their parents’ bed, and being in a non-smoking household. Also, it has long been widely accepted that SIDS is less common with breast-fed babies. But none of these address the fundamental biological cause as to what makes some babies susceptible to a sudden cessation of breathing, followed rapidly by death unless a parent or caregiver is immediately ‘on hand’.

Bovine BCM7 (beta-casomorphin7), which I call the ‘milk devil’, has long been suspected as a villain. This ‘milk devil’, which is an opioid derived from casein (and hence the name ‘caso’ from casein and ‘morphin’ from morphine), is only produced from digestion of A1 beta-casein (1, 2), which itself is only produced by some cows of European breeds. This A1 beta-casein is the consequence of a chance mutation in an ancestor some thousands of years ago (3). Unfortunately this mutated gene is now found in a considerable proportion of European cows.

Scientific evidence has linked bovine BCM7 to many health conditions such as Type 1 diabetes and heart disease (4, 5), child development and symptoms of autism (6, 7).  On the PUBMED database there are now more than 250 peer reviewed medical and scientific papers on casomorphins. However, the evidence that BCM7 might be a major villain for SIDS has, until now, been somewhat indirect.

Back in the 1990s, beta-casomorphins were found in the brainstems of SIDS babies (8). But comparing this with the brainstems of healthy children was obviously not possible. Also, in young rabbits and rats (9) it had been shown that injecting BCM7 into the blood leads to apnoea (depressed and irregular breathing). But obviously these sorts of trials cannot be done with humans. Also, it is only recently that detection kits have become readily available for testing BCM7 in blood.  A further complication has been that in all likelihood some babies are more susceptible than others, but there has been no way to identify the genetic aspect of risk.  In my book ‘Devil in the Milk’ (p152), first published in 2007 (10), I introduced the latest evidence relating to SIDS (11), but at that time there was nothing conclusive.

However, recent work in Poland led by Dr Elzbieta Kostyra, and published by leading scientific and medical publisher Elsevier in the April 2011 issue of the journal Neuropeptides, has provided answers to the major questions (12). There can now be little doubt that BCM7 is a risk factor for SIDS.  Also, it is now clear that the babies most at risk are those who have low levels in their blood of an enzyme called DPP4 (dipeptidyl peptidase 4). This is the only enzyme in humans that can break down BCM7 (13-15).

The Polish work is based on studying babies who have had life threatening events from apnoea, but whom the parents and/ or doctors managed to save. Blood samples from these babies were then compared to healthy babies. Key findings were that the ‘at-risk’ babies had three times the level of bovine BCM7 in their blood as the healthy babies. Also, these at-risk babies had 42% less DPP4 than the healthy babies. Both of these results were statistically significant at p< 0.001.  In other words, the chance of getting a result like this due to random factors, rather than being causatively linked either to each other or a common third factor, is less than one in one thousand.

Analysis of the healthy babies showed that variation of BCM7 within this group was positively associated with more DPP4 activity. In other words, in healthy children the body naturally increases DPP4 activity when BCM7 is high.  But in the at-risk babies the DPP4 level was actually much lower rather than higher. This demonstrates that the at-risk babies are deficient in their ability to quickly respond to high BCM7 by producing sufficient quantities of the only enzyme that can break it down.

The babies were fed on three types of diet, determined by their mothers. Not surprisingly, those fed milk formula that was high in casein had much higher BCM levels than those fed infant formula that was predominantly (but not exclusively) whey. This was to be expected given that BCM7 can only come from casein and not from whey.  However, somewhat intriguingly, babies aged 1-4 months who were apparently being exclusively breastfed also had bovine BCM7 in their blood. How did this get there? The Polish researchers and other scientists have been investigating for quite some time how protein fragments, such as but not only bovine BCM, can get from the mother’s stomach into breast milk. It could be that the BCM7 is being transferred through the blood (16, 17), but it is looking increasingly likely that it might also be via other mechanisms, perhaps including the lymph system.  Regardless of how is it is occurring, there seems little doubt that bovine BCM7 can get into human breast milk, and that it can cause life threatening events in babies. So the evidence indicates that it is not only the babies, but also the lactating mothers, who need to be on cows’ milk that is free of A1 beta-casein.

The Polish work led by Dr Kostyra dovetails very nicely with work by Russian scientists that was published in another international journal, Peptides, in late 2009 (6) . That work showed that babies fed infant formula not only had high levels of bovine BCM7in their blood, but that a proportion of these babies were much slower than other babies to metabolise and eliminate the BCM7. These slow eliminators were at high risk of delayed psychomotor development. The Russian scientists did not investigate the reason why some babies were slow BCM7 eliminators, but an obvious hypothesis would be that they had low DPP4 in the blood.  This latest Polish work now provides strong confirmatory evidence for this hypothesis.

The implications of this work would seem obvious. If infants are to be fed milk formula then it needs to be free of A1 beta-casein. In other words, it needs to come from cows that are what we call ‘A2 cows’ and which produce ‘A2 milk’. Also, lactating mothers would be well advised to not drink milk containing A1 beta-casein. 

My assumption is that the mainstream dairy industry will try and denigrate this research. For example, Dairy Australia has a standard response to any new research on A1 beta-casein along the lines that ‘all milk is the same’.  Of course all milk is not the same and such a statement is scientific nonsense.  So how will they denigrate this research? Detractors might say that it is ‘just one study’.  This was a typical response to the Russian work (6) published in 2009.   They might also refer to the European Food Safety Authority (EFSA) report of January 2009 (1), which claimed there was no proof that BCM7 was getting through from the digestive system to the blood.  Back in 2009 that statement might have been defensible, in that arguably there was strong evidence (which EFSA failed to acknowledge) but not final proof. But now in 2011 that position is no longer tenable.  They may also argue – as was said with the Russian research, which like this Polish research came out of leading scientific institutions – that we do not know enough about their research standards. Well, in that case it is time they went and found out. These are leading scientific institutions. In any case, both the Russian and Polish work is published in highly ranked international  journals following international peer review.

Major elements of the mainstream dairy industry, at least in Australia and New Zealand, have known about BCM7 and the apparent links to a range of health conditions for more than a decade. They hoped that those apparent links might disappear. And for a while it seemed that this might happen. Now, there is no chance that this will happen.

So what can the industry do about it? Well, one thing they could do is breed A2 cows. This is easy to do, using semen that carries the A2 variant of the beta-casein gene. Most New Zealand and Australian bulls already have their A1/A2 status known and recorded. In ten years time the national herds could be close to pure A2, with only inconsequential levels of A1 beta-casein remaining. Then we would have all of our dairy herds the way nature originally intended!  The irony is that we could already be in that position if we had only acted when evidence first emerged.   But because only a minority of farmers have been converting their herds, the industry will now have to work out how to sell ‘A1 milk’ for the next 10 years. That might be a challenge, and hence there will be a continuing industry fightback (‘we must not say anything negative about milk’, or ‘nothing is proven’). There will still be plenty of people who will drink the ‘ordinary milk’ despite the risks, and indeed many of those people may not be susceptible to the BCM7. So ordinary milk will still sell while the change is being made.

However, for parents of young children in particular, the time has come for them to be made aware of the emerging evidence: BCM7, and hence milk that contains A1 beta-casein, is an evidence-based risk factor for a range of childhood health conditions.  SIDS has now moved up that list of conditions. There are options to reduce those risks.


UPDATE: (14 April 2011)

It has been suggested to me that this is all a bit scary. Perhaps it is even scaremongering. The first (i.e. it is scary) I disagree with, and the second (scaremongering) I refute even more strongly. It is SIDS and not this story that is scary. This is a story of hope and moving forwards with solutions. But I do agree that perhaps a little more guidance might be helpful. Some time in the future, and hopefully the near future, it will be possible to purchase infant formula made from the milk of A2 cows. In the meantime the ‘no-cost’ or ‘low-cost’ options to reduce risk are:
1) breast-milk
2) whey-based infant formula (although most of these formulas will still contain some casein).
It seems that mothers who are breast-feeding can further reduce their risk by themselves drinking A2 milk; i.e.milk that is free of A1 beta-casein .  And once the babies are weaned from the breast or from infant formula, then the milk they drink can also be from A2 cows, at least in countries like Australia and New Zealand where A2 milk is commercially available.
Of course for specific advice parents should consult a professional dietitian.

Update: This version was updated 25 April 2011.


Note: the full reference for the SIDS paper is:

Wasilewska J, Sienkiewicz-Szlapka E, Kuzbida E, Jarmolowska B, Kaczmarski M, Kostyra E. The exogenous opioid peptides and DPPIV serum activity in infants with apnoea expressed as apparent life threatening events (ALTE). Neuropeptides. 2011 DOI: 10.1016/j.npep.2011.01.005  ( This is a corrected proof, peer reviewed, and able to be cited, available online to subscribers to the journal, with hard copy and page numbers still to be assigned.)


Other References

1.      Scientific Report of EFSA prepared by a DATEX Working Group on the potential health impact of β-casomorphins and related peptides. EFSA Scientific Report (2009) 231, 1-107.

2       De Noni I,  Release of b-casomorphins 5 and 7 during simulated gastro-intestinal digestion of bovine b-casein variants and milk-based infant formulas. Food Chemistry 2008; 110:897-903

3.     Ng-Kwai-Hang KF, Grosclaude F. Genetic polymorphism of milk proteins. In: Fox PFaM, P.L.H editor. Advanced Dairy Chemistry: Volume 1: Proteins, Parts A&B. New York: Kluwer Academic/Plenum Publishers; 2002. p. 739-816.

4.     Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth HE. Type I (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption. Diabetologia. 1999 Mar;42(3):292-6.

5.     Laugesen M, Elliott R. Ischaemic heart disease, Type 1 diabetes, and cow milk A1 beta-casein. N Z Med J. 2003 Jan 24;116(1168):U295.

6.     Kost NV, Sokolov OY, Kurasova OB, Dmitriev AD, Tarakanova JN, Gabaeva MV, et al. Beta-casomorphins-7 in infants on different type of feeding and different levels of psychomotor development. Peptides. 2009 Oct;30(10):1854-60.

7.     Cade JR, Privette MR, Fregly M, Rowland N, Sun Z, Zele V, et al. Autism and Schizophrenia: Intestinal Disorders. Nutr Neurosci. 2000;3:57-72.

8.     Pasi A, Mahler H, Lansel N, Bernasconi C, Messiha FS. beta-Casomorphin-immunoreactivity in the brain stem of the human infant. Res Commun Chem Pathol Pharmacol. 1993 Jun;80(3):305-22.

9.     Hedner J, Hedner T. beta-Casomorphins induce apnea and irregular breathing in adult rats and newborn rabbits. Life Sci. 1987 Nov 16;41(20):2303-12.

10     Woodford, K. ‘Devil in the Milk.  Craig Potton Publishing 2007. (Updated Edition 2010, American Edition published by Chelsea Green 2009)

11      Sun, Z., Zhang, Z., Wang, X., Cade, R., Elmer, Z., Fregly, M., Relation of betacasomorphin to apnea in sudden infant death syndrome.   Peptides.  2003;  24,:937–943

12.   Wasilewska J, Sienkiewicz-Szlapka E, Kuzbida E, Jarmolowska B, Kaczmarski M, Kostyra E. The exogenous opioid peptides and DPPIV serum activity in infants with apnoea expressed as apparent life threatening events (ALTE). Neuropeptides. 2011.

13.   Nausch I, Mentlein R, Heymann E. The degradation of bioactive peptides and proteins by dipeptidyl peptidase IV from human placenta. Biol Chem Hoppe Seyler. 1990 Nov;371(11):1113-8.

14.   Kreil G, Umbach M, Brantl V, Teschemacher H. Studies on the enzymatic degradation of beta-casomorphins. Life Sci. 1983;33 Suppl 1:137-40.

15.   Tiruppathi C, Miyamoto Y, Ganapathy V, Roesel RA, Whitford GM, Leibach FH. Hydrolysis and transport of proline-containing peptides in renal brush-border membrane vesicles from dipeptidyl peptidase IV-positive and dipeptidyl peptidase IV-negative rat strains. J Biol Chem. 1990 Jan 25;265(3):1476-83.

16.   Iwan M, Jarmolowska B, Bielikowicz K, Kostyra E, Kostyra H, Kaczmarski M. Transport of micro-opioid receptor agonists and antagonist peptides across Caco-2 monolayer. Peptides. 2008 Jun;29(6):1042-7.

17.   Shimizu M, Tsunogai M, Arai S. Transepithelial transport of oligopeptides in the human intestinal cell, Caco-2. Peptides. 1997;18(5):681-7.


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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36 Responses to BCM7 and Sudden Infant Death Syndrome

  1. Elfnow says:

    I take exception to the idea that correlation equals causation here, especially with respect to very specific ailments (Type 1 Diabetes, Autism, etc).

    I don’t take exception to SIDS, as I don’t believe it’s a single issue in all cases.

    There have been studies that indicate that consuming 1.5 to 3 alcoholic beverages PER DAY is correlated to being 30-60% less likely to be a “healthy weight” (not obese) in twenty-something-aged women. You can’t even begin to sell me on the idea of drinking that much, even if I clearly am obese and don’t drink very often at all…

    I worry that your readership confuses correlation and causation, especially as you present the information as though there is a causative effect, especially with respect to specific ailments.

    Personally, I think that if there IS a response to βCM-7 it’s due to its similarity to histamine, not because it is “like heroin”, as I’ve seen referenced (not here, but in other places), but rather because it acts like histamine when no allergen is present. It’s an interesting thought.

    In any case, I’m doing my part… while I don’t think it’s a cause of autism directly (no, you can’t tell me it crosses the blood-brain barrier…sorry) but I imagine that it might establish a cascade effect. In any case, selective breeding of cattle limits the gene pool even further (blah!) so I’m looking into alternative casein sources.

    Just be careful about correlation. Causative agents, especially in humans, are notorious to pin down. Like life, it’s all about the path you take, not where you start. 😉

    • Keith Woodford says:

      Your comment is wide ranging. I am not going to get drawn into issues such as the relationship between alcohol and obesity. But I will respond to the issue of correlation and causation, and how that issue relates to BCM7 and SIDS.
      You will note that I did not use the term ‘causation’. That was purposeful. But I did use the term ‘risk factor’ in a way that was scientifically and medically appropriate given the data.
      We all know (or should know) that correlation is capable of misuse. This is particularly the case with time series data where lack of independence in the data, serial auto-correlation, and ignoring of third factors, lead to ridiculous correlations that have no meaning. For example, it is possible to find meaningless correlations between the number of televisions in the world and any other factor that has been increasing over time (such as AIDS). Such analyses do not get past the referees and editors of reputable journals such as Neuropeptides.
      The methodology in this Polish research is called case-control. It is a well-regarded methodology in epidiemiology. In ths research, the cases are the babies who had acute life threatening events (ALTE). The controls are babies that are carefully selected according to factors such as age and socio-demographics to be used for comparison.
      The analysis is based on analysis of variance (ANOVA). Case-control is a particularly effective and efficient methodology for conditions, such as SIDS, which have a low incidence in the population.
      All of the current recommendations for SIDS, such as babies sleeping on their backs rather than their tummies, and parents that don’t smoke, are based on case-control and similar methodologies. There has never been and there never will be a double blind trial where some babies are put to sleep on their backs and some on their tummies. It would not get past human ethics and the mums would never agree. In fact some of the techniques that have been used are less sophisticated than case-control. But that does not mean that they have not been good studies. Indeed the recommendations from those studies have led to many lives being saved.
      In well conducted studies, the relationships are analysed for statistical significance. With this recent Polish research, the statistical significance is P<0.001. This means that there is less than one in one thousand chance of getting a result like this (that ALTE babies have three times the level of BCM7 in their blood of other babies) without this result also having meaning in the underlying population of babies. It also means that criticisms such as the 'the sample is too small' are nonsense.
      The next issue is therefore to ask as to precisely what meaning can be taken from the results. In theory there are three possibilities.
      a) The life threatening event is caused by the high BCM7
      b) The high BCM7 is caused by the life threatening event
      c) The life threatening event and the high BCM7 are both caused by a third factor with which both are closely associated.
      Note that the other possibility, that the relationship is a fluke and non repeatable, has been excluded at the level of being less than one chance in one thousand.
      So let's look at alternatives b) and c) before coming back to the first alternative.
      The likelihood of the life threatening event leading in itself to subsequent high BCM7 has no known theoretical or biological logic to it. But it cannot be totally excluded, and I am therefore open to this notion. Even if this were the situation, and given what we know about BCM7, it would be a real worry knowing that these chidlren had three times the level of BCM7 consequent to their life threatening event.
      The likelihood that the ALTE and the high BCM7 are both associated with a third relevant factor is a serious possibillty. Indeed the data is pointing very much in this direction. That factor is low criculating DPP4 in the blood. Remember that DPP4 is the only enzyme that breaks down high proline-containing peptides such as BCM7. So there is real scope for a serious debate as to what has 'caused' the ALTE. Is it the low DPP4 or the high BCM7? However, casting the problem as 'either/or' is not helpful. Solving either problem (high BCM7 or low DPP4) will reduce the risk, but it is much easier to remove BCM7 from the diet than it is to genetically re-engineer the baby!. So that is why I talk of BCM7 as a risk factor.
      In labelling BCM7 as a risk factor, it is also important to note that these Polish results did not come out of the blue. There has been peer-reviewed evidence in the scientific literature for more than 20 years linking BCM7 to apnoea and SIDS. The power of this paper is not just finding the BCM7 in the blood (although that is very important), but finding that the susceptible babies are those with low circulating DPP4.
      The additional finding that bovine BCM7 is apparently getting from the mother's stomach to the baby's stomach via the mother's milk is also very important. This should lead to some very interesting ongoing research.

  2. Bron jaenke says:

    Mr Woodford i would personally like to Thank you for the information you have made available to us as consumers. It is understandable that many people will refute the possibility of the ‘milk devil’ but to me the proof is the change in health of my family. Word is slowly getting out, i can also tell you as we were told of the benefits of a2 milk by a regional health care nurse and we have never looked back. It also helps that my family have autism, type 1 diabetes, and many other auto immune diseases that have seen a considerable improvement on since the switch to a2. This isn’t just about us but our children and their children’s future. Keep us the good work, its now becoming important to us the regular families, that you speak on our behalf. Best wishes, Bronwyn Jaenke.

    • Keith Woodford says:

      Thanks Bronwyn.
      By my reckoning there are now more than 600,000 Australians who are regularly drinking A2 milk. That number increases every month as the word spreads. It is a combination of new science continually coming through, plus word-of-mouth from existing consumers to new consumers. This last weekend I have been across in Sydney talking to health professionals, and the level of awareness amongst them is rapidly rising. It is considerably higher than when I spoke to a similar group in Sydney one year ago.

  3. Bron jaenke says:

    Just out of interest i was reading an article about using naltrexone to treat chrohn’s disease sufferers inflammation with some success. Could this also be linked to BCM7?

    • Keith Woodford says:

      Yes. Naltrexone is an opioid antagonist, i.e. it reduces or removes opioid effects by attaching to the opioid receptor itself and making these receptors unavilable for the opioid to attach to. There is an increasing understanding that immune diseases relate to opioids messing up the bodies immune system. Internally generated opioids (endophins) are important in relation to immune system messages, but opioids in food (exorphins)such as gluten and BCM7 can swamp the messenger system. Naltrexone is now being used at low doses for a range of immune conditions.
      So yes, naltrexone will reduce the effects of BCM7. But, as with all drugs, it can (and does)have its own side effects.

  4. Edward Miller says:

    Woodford makes a strong case for using non-A1 type milk or casein in baby products.
    As you might gather I am looking for ways small changes might produce big public health benefits. Alternatives to A1 beta casein containing milk formulas include human milk (best), or formulas including soy, whey, goat milk, or A2 beta casein. Baby formula appears to be one where replacing relatively small quantities of A1 type beta casein with A2 type beta casein would have significant health benefits.
    Alas, no baby formula or other casein products that state they are free of A1 beta casein appear to be on the market. A2 Corporation has stated they hope to change this. Providing such a product appears to be potentially a money maker since baby formula is fairly expensive per pound and babies being small do not consumer many pounds of it per day. Many mothers are very protective of their babies health and should be willing to pay a premium price for such a product. Is there a way to increase the use of such alternatives and to encourage the introduction of new formula formulations.
    Perhaps the optimum political strategy is to lobby for A1/A2 informative labels, and especially Infant Formula labels to state how much beta casein of type 1 is included. Current US formula labels do not revealed how much A1 type beta casein they contain. My understanding is that tests are available that can tell you how much beta casein of the A1 type is included. They appear not to be protected by patents, since the existence of these beta-caseins has been known for years. Am I right on this point?
    This would be similar to the technique used with trans-fats to reduce the public’s exposure. Once the percentage of trans fats was being included on US labels, many firms figured out how to reduce this percentage, or even eliminate trans fats completely. This elimination of trans fats involved real costs, either financial or in terms of taste.
    Once the amount of beta casein in Infant formula was being revealed on labels, it is likely brands would be introduced with zero percent, or a very low amount. This would be done either by not using cow milk at all, or by using whey, or by using milk solids imported from countries where Zebus or other Bos indicus breeds provided the milk, or by contracting with farmers to provide milk from herds selected not to produce A1 type beta casein.
    In the course of discussions leading up to this the public would be educated on the A1/A2 issue. There would very likely emerge a demand for other products, including liquid milk, that were low in A1 beta casein, or free of it. Where casein was user as a binder (certain nut bars possibly) one might expect to see casein imported from countries with Bos indicus cattle. This might also lead to the introduction of A1 free milk, whether by taking a license from A2 Corporation, or just producing it and selling it under another brand name.
    If need be, these firms might wish to call A2 Corporation’s bluff (if it is one) and litigate the validity of their patents (or pay for a reexamination), which appear to be very vulnerable. Their inventions appear to lack the required originality. They start with a scientific discovery concerning the possible effects of different types of beta caseins (these discoveries appear to be non-patentable in themselves). An implication of these discoveries is that milk of certain types may make one less likely to suffer from certain diseases. They then claim as an invention the very obvious idea of not mixing the more dangerous types of milk with the less dangerous, and consuming the safer milk. This idea is rather obvious, and it has been known for many years that if one has some milk that may be dangerous to drink (say due to contamination), that the dangerous milk should not be mixed with less dangerous milk, and that one way to produce a safer milk is to keep less safe milk from being mixed with it.
    Their patents also involve the well known technique of selective breeding to produce more animals whose milk has the desired traits. Breeding is to eliminate an undesired trait is obvious (at least to one who knows Mendelian genetics) and selective breeding is a technique that has been known for years.
    Their patents do not mention sudden infant death syndrome, and they do not also discuss the techniques for producing milk that can be advertised as low in bovine beta casein 2, not to protect against a specific disease, but merely because some consumers prefer such milk (or possibly a government regulation even requires such milk).

    Infant formula may be a good product to start the effort to reduce the amount of beta casein consumed in the US. The total tonnage is relatively small, and the powdered version of the product is transportable without refrigeration. Mothers are very anxious the give their babies the healthiest formula they available, and many will pay a premium for it. If just a small percentage of a nation’s market was captured by such a formula, the product could be profitable. Here it differs from fresh milk where the need for refrigeration and the weight (milk is mainly water of course) limits the area that can be served by any single factory.
    There are obvious marketing problems in convincing someone in the US or New Zealand that they should use baby formula from India (or with Indian milk solids) rather than a locally produced one, but it seems to be true. There could be political issues as the industry tries to convince the government that local producers can meet the need. they can be expected to argue that New Zealand, need not be turning to India to feed its babies. New Zealand farmers are capable of producing healthy milk, and New Zealand firms have the technology to process it. Probably the best answer is to say that importing formula, or using imported milk solids would be a temporary measure to test the market, and that eventually local farmers and producers will prove competitive (as I am certain they would). One New Zealand firm (A2) has a head start in producing such a product. New Zealand even has Prof. Woodford, a resource that other countries lack.
    It would seem that there would be a market for a low A-1 baby formula product and the natural question is how would it be produced. Options include goat milk (too little), whey based formulas, soy bean based formulas, or ones whose beta casein contained very little of the A1 type.
    Soy based formulas apparently have problems (they are not legal everywhere, although readily available in the US). There is too little goat milk available to be very useful although I notice Meyenberg (US seller of goat milk) in their literature aimed at doctors does discuss its usage in feeding babies.
    I know little about the merits of whey based products versus others, or even what brand names they are sold under. Most protein in whey is lactoalbumin (either alpha or beta) and some is serum albumin. I do not know enough to know if all of the essential fatty acids are found in the optimal proportions in cow whey. I am inclined to believe they are not since whey appears to be a cheap milk fraction (left over from cheese making), and I think it would be used in baby formula rather than milk if it was suitable.
    Human milk is 60% whey and cow milk only about 20%. If the whey from the two species are similar, there would appear to be scope for using much whey in baby formulas. Of course, even if whey is missing some desirable fatty acids, there may be other ingredients besides milk that could be used to provide them. Alas, I lack the expertise now to know how to formula baby formula, but even if some casein is likely to be in most whey based formulas, they presumably have less BCM7 than others. One issue is finding out what is in formulas under current labeling procedures. Looking at the brand Similac Advance, I can learn that the most important ingredient is Nonfat Milk and that it also includes Whey Protein Concentrate (the sixth most important), although the exact percentages are not revealed. this information makes it hard to guess how much A1 beta casein is contained. Hence, if Prof. Woodford could provide brand names of whey based formula, it might be helpful to someone with a baby. .
    Zebu and other Bos indicus breeds appear to have very little A1 beta casein. It is possible that formulas made outside of Europe, North America, Australia, or New Zealand might be based on milk from breeds that would be very low in a-1 beta casein. India would appear to be a possible source since they are the world’s large milk producer and most of their milk would be low in A-1. I do not know much about their industry (although a web search did show there were firms offering casein for sale). I know little about the legal problems involved in importing from there either for personal use, or for resale. Exporting to the Western markets would appear to be a profitable opportunity for their firms since baby formula (in powder form) does not have to be refrigerated and is fairly valuable per pound.
    I would suggest China as a possible source (presuming most of their cattle were Bos indicus), but their recent scandals (well publicized) involving melamine in milk would make marketing a milk product from there difficult.
    Presumably, formula firms located in the US or Europe could import casein or milk solids from India (or Pakistan, or other countries with Bos Indicus cattle), do some quality checking, and then produce the formula in the US or Europe (or even New Zealand or Australia).
    If the major Western baby formula firms lost even a little market share (or there was unfavorable publicity) one might expect them to start using non-A1 milk in their products (whether imported from Bos indicus countries) or produced nearer home. I saw references in a story illustrated not by pictures of a cow, but of Prof. Woodford, (http://www.stuff.co.nz/business/49646) to reports of Abbot negotiating many years ago for large quantities of powder from Fontera (when they were thinking of going into the business of selling non-A1 milk powders, I presume) although the story stated they did not know if the reports were true or false. Are any of the big worldwide baby formula producers actively looking into such products? It would seem wise for them to be at least looking into such products, or possibly already producing them.

    • Keith Woodford says:

      Whey-based infant formulas are available. This is particularly the case for ‘starter’ formulas for babies less than 4 months of age. But most of these still contain some casein. (In most countries I think it is unlikely that any brands available from supermarkets would be 100% whey.)
      Although the existing evidence can be considered compelling (including another paper from Poland that I have yet to post in relation to BCM5, a derivative of BCM7) there is need for confirmatory evidence from ‘Western’ countries that BCM7 is indeed getting through into the blood before either the major companies or regulatory authorities will be willing to do anything. (In the ‘West’ we are biased againt research coming out of Eastern Europe.) But the major companies do have a watching brief on what is happening. When EFSA reviewed the evidence in 2008, it was the absence of ‘proof’ that BCM7 was getting through into the blood that allowed them to downplay the risk.

  5. Kurosh K says:

    Ms. Woodford,
    thank you for the article – it is reassuring to know we are on th eright track as we are already drinking a2 milk – now this whole notion of drinking it has infrastructural issues – by that i mean how many cows do you think we have that are capable of producing the a2? and let’s say that we are convinced as a whole society that it is the way to go then how do you pursue switching over such mass quantities? or what would be a good alternative to the a2 for all?

    • Keith Woodford says:

      Kurosh K:
      It would take about 10 years to convert all herds to A2 if, as a society, we decided that was the way to go. The key is for farmers to use bulls that have been tested as having double copies of the A2 variant of the beta-casein gene. Most farmers mate most of their cows by artificial insemination, and it is not difficult for these companies to supply A2 semen. For the national milk supply to be pure A2 would be best, but every one percent reduction in the level of A1 beta-casein can be considered a minor victory.

  6. Warwick Chapman says:

    Keith Woodford,
    DEVIL IN THE MILK I found interesting reading. I have started using A2 milk
    and also adding lactase drops to it as my wife is lactose intolerant.
    About 10 yearsago I read a book by Professor Jane Plant called
    YOUR LIFE IN YOUR HANDS Virgin Publishing about breast cancer and
    its relationship to milk in particular. I cannot help but theorize that BCM7 or
    BCM5 may be the missing link that PLANT could not find. The relationship to
    wealthy western countries and milk products being similar.
    Do you know of any research into this

    • Keith Woodford says:

      I am aware of Jane Plant’s investigations, and it is time I went back and had another look at her ideas. I would need to do that before commenting.

  7. Edward Miller says:

    This new research suggests that a strategy for introducing non-A1 milk might go through the powdered milk and milk products route, including baby formula.

    The attempt to introduce the A2 brand in the US appears to have failed. It is hard to figure out why or how, but a web search showed the little mention of it in the press was in local papers, probably working off of the firm’s press releases. It appears the strongest claims they felt they could safely make was that it was certified to contain a minimum quantity A2 beta casein (rather than being low in A1 beta casein), better “digestibility ” for some people, and environmental friendliness (it was being bottled in a biodegradable contained made by a firm that has changed names and is now pushing bottled water). There was only one mention of very little A1 beta casein (claimed 99% free of A1 beta casein). It is not surprising that such a product did not sell, especially if it was premium priced. If you know more of why it failed, it would be interesting to know.

    The number of consumers for whom A2 beta casein meant anything must be small judging from the absence of discussion of the issue in the US, and the small sales of Devil in the Milk book. The high cost of transportation and the need for refrigeration of liquid milk limited the geographic area over which the product could be made available, and apparently there were not enough informed customers to support the product.

    A dried product could be sold over the United States and sales made by internet, delivered by post office or parcel post. In the whole US (and perhaps a few foreign countries) there may be enough consumers for whom low A1 beta casein means something to support production. New Zealand or Australian firms already making A2 milk under license might even be able to sell into such a market. I believe the US has a quota system in which imports of milk powder are restricted. However, if the New Zealand product was one product that was low tariff for the US or it could somehow come in under the New Zealand quota, such as casein or protein powders, it might be possible to sell it in the US.

    This way a suitable casein source for the baby formula industry might be possible. I am not certain why the whey based formulas still have casein in them, but a plausible guess would be that certain amino acids are not present in adequate quantities in whey (which I believe is usually cheaper than milk or casein). While there may be non-milk ways to get these amino acids into a baby formula, purchasing the required quantity of A2 casein (which may are may not be bought as a powdered milk product, bringing along whey proteins) would be one way, and probably affordable. As I mentioned earlier, if this could come from a Zebu breed as casein or powder from India, the need might be met also without worries about A2 patents.

    Given the high price of formula (per pound), the evidence that A1 beta casein creates problems, and the concern many mother’s have about the health of their babies, one would certainly think that a product free of A1 beta casein could find a market (although soybean based formulas could be a problem in countries where they are offered).

    • Keith Woodford says:

      The marketing of A2 milk in USA failed for multiple reasons. First, it is very difficult to market a product where the value proposition is complex. Also, consumer legislation limits the ability to claim health benefits. Further, the business structure appeared to have too many people clipping the ticket along the way. By contrast, A2 milk is being marketed very successfully right across Australia despite the same constraints of difficulty ion communicating the value proposition in simple terms, and restrictive consumer legislation. The big difference is that in Australia the issue has received considerable TV, radio and press coverage at opportune times.

  8. Foster Kalma says:

    After discussing A2 with you in May I am now reading Devil in the Milk. I am fast comming to the conclusion I must convert my herd to A2A2 out of a moral obligation to produce the healthiest milk I can. I also want to avoid feeding BCM7 to my family. I don’t see an immediate market benefit available through my existing dairy company.

    I have spent this evening looking through the lists of bulls to see what status the bulls I have used from the major semen supplier over the last years is. I was happily supprised to find about 90 percent are A2A2. Several A1A2 bulls seem to have been added because their Breeding Worth was too high to ignore. Several of the bulls are even marketed highlighting A2A2 as their primary advantage.

    The conclusion I draw is that they will “never do anything that destroys the (milk) catagory” by admitting there is a problem, but in the background breeding companies are working hard to breed A1 out of our national herd.

    So given we are probably between 3 and 5 years down the road of passively breeding towards A2A2 what do you consider the value of me DNA sampling my herd and young stock now to remove the A1 stock faster?

    • Keith Woodford says:

      Hello Foster
      In general, I advocate strongly that farmers should use A2 semen as a risk management strategy, but I am cautious in suggesting that they DNA test their cows. This is because there is quite some expense and no guarantee of a quick return on that investment. Having said that, if I were farming, and in the current economic climate, I personally would test. In part that would be because I think there will be a return down the track, but in my case it would also be because of the satisfaction I would get from increasing the A2 content of the herd as quickly as possible. In your case, with your herd already likely to be high in A2, it will be hard to go the next step without testing.
      For a 400 cow herd it would presumably cost about $10,000 to test the whole herd. Assuming you were to use only A2 semen, then progeny of A1A2 cows would still need to be tested to see if they are A1A2 or A2A2. For farmers who are already DNA testing the calves then the additional cost should be minor.
      Currently I am maintaining a low profile here in NZ in relation to A2, but confident that the time will come when the tide turns. I am very confident about the final outcome, but not so confident as to the timing as to when that tide will turn. At some future time there will be a real scramble for A2 milk. And there will be a real premium on A2A2 heifers.
      There are a few bulls showing up in NZ as neither A1 or A2 but as B. This is mainly in Jerseys. There is new evidence that the release of BCM7 from the B beta-casein is even greater than from the A1 beta casein. I have pointed out to an LIC director that they have a couple of these bulls in the stable but have heard nothing back.KeithW

  9. Edward Miller says:

    At this time I believe the New Zealand patent of A2 Corp. on testing is expired due to non-payment of fees, but I expect it will be granted a renewal. If concerned about A2 learning things about you or your herd, you may be in a good position to ask the information not be revealed, or possibly to get a better price on testing.

  10. Edward Miller says:

    There is considerable material on dipeptidyl peptidase IV (DPP IV) in the book Biological Treatments for Autism and PDD by Dr. William Shaw 2008. You can find it on Amazon and by searching inside the book read part of it before laying out the $25 US dollars for it.

    I notice from p82 that his lab offer tests for casomorphin in the urine. He also talks a lot about casomorphin and a casein elimination diet but seems unaware that there is some milk which will not produce certain types of casomorphin during digestion. He has a nice chart on p80 as to which peptides are activate or inactivated by DPP IV.

    The link is http://www.amazon.com/Biological-Treatments-Autism-William-Shaw/dp/0966123859/ref=sr_1_5?s=books&ie=UTF8&qid=1309910990&sr=1-5#reader_0966123859

  11. John says:

    I had a friend that told me that in japan they increased the age for vacination and when they did that the age that cot deaths happened also increased. Don’t know if that is true or not.

  12. Edward Miller says:

    Got Milk and Baby Formula

    Your discussion leaves out the goat milk alternative as a way to avoid the problems with A1 beta casein.

    Goat milk is available in most countries, so others can drink the ilk to avoid BCM7 in their milk.

    The goat milk alternative is important because there do appear to be goat’s milk formulas on the market in some countries, while it currently appears there are no A2 based formulas on the market. The absence of A2 type powder on the market may prevent such a product from being quickly produced.

    In New Zealand there is Karicare Goat Starter Formula (see http://www.nutriciababy.co.nz/main/nutrition/karicare_goat_starter_formula_12.html). Their web site makes no reference to avoiding the problems of BCM-7, but merely to “a naturally soft curd” that may be easier for babies to digest and “a high proportion of medium chain fatty acids.”

    They also have a Karicare Goat Follow-On Formula. They also offer cow milk based products that they claim are the only whey based products on the New Zealand market. Although it is not clear from the web site, I assume there is still some casein in these whey based products, which would imply some potential for a BCM-7 product.

    Karicare is produced by Nutricia. Nutricia New Zealand Limited is part of Group Danone, Numico, bought recently (2007) by Group Daneone is the direct owner of the Nutricia brand.

    In Australia there is “Karicare Goat 1 from Birth”, which they describe as designed to meet the needs of bottle fed infants from 0-6 months.

    They also have a “Karicare Goat 2 from 6 months (Follow-On).”

    I presume if these products could be sold in New Zealand and Australia, similar products could be formulated for other countries.

    A firm called Health Life New Zealand ships Karicare all over the world. They do list Karicare Goat Starter Formula 1 (US $ 48.04) , Nutricia Karicare Goat Milk Follow On Formula (US$48.04), Karicare Toddler Goat Milk Powder Step 3. (US $ 49.70). I tried a one container order to see if they would ship to the US, and it accepted the order, with a NZ post of $24.85 (or 57.99 for EMs Express). (see http://www.healthlifenz.com/en/Karicare-toddler-goat-3.html).

    Thus, it looks like that for consumers who are willing to pay, there is safe baby milk product available.

    At a cheaper price an internet search turned up a product described as follows:

    • “perfectlyhealthy Best Toddler & Child’s Goat Milk Formula – Chocolate – 16 oz.
    perfectlyhealthy Best Toddler and Children’s Goat Milk powder for ages 1 through 8 is a nutrient rich synergistic blend of goat milk protein, colostrum, probiotics, EFA’s, Flax Seed and Vitamin D3. Formulated by Leigh Erin Connealy, MD to reduce allergy symptoms and provide a product closest to mother’s own milk. This is a nutrient rich protein drink for toddlers and kids! This supports prevention of diabetes, allergies due to dairy products or cow’s milk, obesity, ADHD, and may prevent Coronary Heart Disease later in life. This comes in 16 ounce green friendly jars – approx. 13 daily servings. Organic Chocolate and Vanilla Flavors!”

    Note some of the claims suggest they are aware of the BCM-7 issue. It is priced at $29.99 (diapers.com price) and ships from within the US.

    An internet search also turned up a product described as:

    “Bambinchen Infant Formula is produced on the basis of goat’s milk protein.

    It is a full-fledged dietary infant formula, accommodating babys needs.”

    It is priced at 11.95 euros.

    In Britain, one product on the market is “Nanny Care,” which I understand is the same product as Karicare ,which is marketed in New Zealand. It is marked by Vitacare and the goat milk reportedly comes from Dairy Goat Cooperative in New Zealand.

    There was an effort to get goat milk protein approved in the European Union (whose rules also controls in the UK). It failed due to failure to prove it was equivalent to cow based formula in baby growth.
    The EFSA statement (2006) is at (http://www.efsa.europa.eu/en/efsajournal/pub/30a.htm). The essence of the problem was not that any real problem was found with goat’s milk , but that the sample size was inadequate to prove that equivalent growth was achieved. Some issues were originally raised with regard to amino acid composition, but were apparently resolved.

    The controversy is discussed at http://www.wddty.com/nanny-state.html. There is a Telegraph article from 2005 (http://www.telegraph.co.uk/news/uknews/1492334/Goats-milk-formula-not-suitable-for-infants-Government-warns.html) in which the UK government came out against goats milk in formulas.

    With the new evidence on BCM7 it appears to me that a new effort is called for in the European Union. If one just compares goat milk to human milk, it appears closer to human milk than cow’s milk in general.

    There are several official recommendations against goat milk, but most of them appear to be against using goat milk alone, rather than as a formula ingredient. For instance the USDA has such a statement (see http://www.nal.usda.gov/wicworks/Topics/FG/Chapter4_InfantFormulaFeeding.pdf). For instance, there seems to be general agreement that both goat and cow milk contain too little iron for use in infant formulas, and additional iron should be included. The US infant and children’s program (which subsidizes about half of the formula purchases allows states to permit goat milk purchases, but apparently many do not allow it, probably because of the higher cost).

    From a political viewpoint, if a goat milk formula is marketed, it might lead the cow milk based formula firms to decide to meet the competition with a product free of A1 beta casein type. Possibly, if they perceive a threat from goats milk, they might decide to fight it by bringing out a A2 milk type product on their own. While if a push is made initially for an A2 type product, they may back themselves into denying that there is a problem, a position it may be hard to get them off of.

    In the long run, a A2 type cow milk product will probably win because it can be produced more cheaply. However, no A2 powder is now on the market, and goat milk powder is. In some countries, A2 patents may present an obstacle to firms that want to produce an A2 cow milk formula. Goats milk should be available.

    There is also an article on preparing homemade goat milk formula at: http://www.ehow.com/way_5476022_homemade-goat-milk-baby-formula.html

  13. Edward Miller says:

    Dipeptidyl peptidase IV

    There is a whole book Dipeptidyl Aminopeptidases by Lendeckel, Reinholdt and Bank (2006). While the subject is complex, one thing is clear. DPP-IV acts on a vast number of peptides in the blood, and many of these have important regulatory roles. An obvious speculation is that the presence of BCM-7 in large quantities affects some of the other uses in the body for this enzyme, and has assorted effects, although it is not clear what these are. Since it has been possible to use DPP-IV inhibitors in the treatment of diabetes, these effects may not be major, but the issue does not appear to have been fully investigated.

    As Woodford has pointed out, inhibiting DPP-IV in the treatment of diabetes may leave the patent more vulnerable to any arteriosclerosis effects of BCM-7. Given the possibility of detecting BCM-7 in the blood, it should be possible to investigate whether drinking A1 beta casein containing milk has an effect, and if it does to monitor the patients for effects, possibly by monitoring carotid artery intima-media thickness.

    Wikipedia reports that one such drug, Sitagliptin, is a competitive inhibitor of DPP-IV. Possibly BCM-7 cold also inhibit the action of DPP-IV by binding to it. If this is the case, the effectiveness of the drug may be influenced by how much and what types of casein the patient consumes. Possibly, investigating this may be a way to get more research on BCM-7 done. Since BCM-7 is believed to have a role in type 1 diabetes, this may be it easier to get diabetes researchers interested.

    The Polish study discussed here suggests that the levels of DPP-IV increases with the amount of BCM-7 in babies. If a similar effect occurs in adults, milk consumption might have an effect on the levels of the enzyme, which in turn might affect the required dose of DPP-4 inhibitors.

    An obvious testable implication of the theory that BCM-7 get into the blood stream and is atherosclerotic, is that coronary artery disease problems including heart attacks should be more common in those diabetes patients being treated with DPP-4 inhibitors than in those being treated in other ways. This is a study that should be done.

    Since high blood pressure is an effect of atherosclerosis and is frequently treated by drugs, it may be possible to do such a study from records of prescriptions written, presuming milk consumption is the same in both groups. Are those given DPP-IV inhibitors more likely to also be prescribed high blood pressure medications than those with diabetes treated with other drugs? If an effect is found, more elaborate studies might be attempted, starting with questionnaires that investigated milk consumption.

  14. Alan Burton says:

    Mr. Woodford,

    I would like to express the greatest gratitude I can to you for your diligence in spreading this valuable information. It has meant a great deal to my family since my son experiences disruptive tics when he consumes too many mass marketed milk products. He does not experience these effects when limited to milk products purchased directly from a dairy (our only source here in the States) with exclusively Guernsey cows. If it were not for your work we would have never become aware of the benefits of A2 milk or have been able to observe these benefits so directly. Furthermore, since he is at risk for type 1 diabetes we are hopeful that we are dodging a bullet. I can add that we have tried the dpp-iv without observable benefits but that assisting the detoxification pathways in the liver with niacin, magnesium, and a few other vitamins has also been quite useful but no substitute for avoiding bcm-7.

    Alan Burton

  15. Peter says:

    In one of their studies, Sokolov and Kost in Russia showed that BCM7 blocks serotonin (i.e. 5-HT2) receptors in rats’ brains.
    Jhodie Duncan (from Australia, when she was in Boston) and other Boston SIDS researchers
    found that lack of serotonin is common in babies who died of SIDS. Ref: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3242415/ ,
    also reported at http://www.boston.com/community/moms/articles/2010/02/02/scientists_link_serotonin_deficit_to_sids/.
    I think they wondered what might be blocking the serotonin receptors. I can guess the answer.
    I think researchers in Ireland and Italy have made similar findings to Duncan et al.
    I also read somewhere that all babies have periods of sleep apnea, and it is serotonin which makes such periods of apnea (apnea = not breathing) cease, i.e. the cessation of apnea, and resumption of normal breathing, is one of serotonin’s roles.
    Do you know if anyone in the world is putting these sorts of ideas together in order to try to solve just what SIDS is?

    • Keith Woodford says:

      There is a group in the US that is working on the effects of BCM7 at the cellular level. They appear to be making good progress but they have yet to publish their results.

  16. Austin Driscoll says:

    Keep up the great work. Can you tell who is doing the work on BCM7 at the cellular level.

    • Keith Woodford says:

      I would like to, but that might get me into some trouble as I am not sure they have announced their line of research. We will just have to wait until they go public.

  17. Peter says:

    In response to John’s comment about increasing the vaccination age in Japan, I’m convinced that idea is wrong, ref http://www.drwile.com/lnkpages/render.asp?vac_SIDS and other sites.

  18. Roland says:

    Dear Mr. Woodford and readership,

    In relation to not only SID, but other likely to be BCM7 related illnesses, conditions: you mentioned in the book there is no thus-far-identified parallel running causation, that would show similarly strong correlation with, but how about the possibility of geopathic stress?

    Reading into this http://www.landandspirit.net/html/body_geopathic_stress.html dedicated site one could find reasoning the likelihood of which to be true is perhaps more imminent to laymen like myself than to specialized scientists who may consider it “anecdotal” even at the brink of 2014.

    It’s worth checking it out. It does not take a bit away from the deliberation you are putting forth in the book. It simply shows how interwoven cause-effect relationships are on Earth.

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  21. Margarit Gut says:

    Hi Keith,
    in our herd of Friesian and Kiwi Cross Cows, we have been using A2A2 Bulls exclusively since your book the “Devil in the Milk” was published. And for or the last few years now, we have been DNA testing our calves and sell the ones that are not A2A2. Our herd is still not completely A2 but it should not be long now.
    At the start we had a few problems with LIC making mistakes in the DNA testing of Bulls, but that has much improved now and they have even started to highlight A2 Bulls in the Bull Catalogues now. We have been told that if two Bulls are almost identical they would choose the A2 Bull over and A1 or an A1A2. Unfortunately they are still using A1A1 Bullsl, which will slow down the move of the National Herd towards A2A2.
    Every so often we are wondering what’s the point of it all, as most other farmers think we are a bit nutty doing this, but then along comes another one of your articles which confirms to us again that we are on the right path. So thank you for your encouragement and keep up the good work.
    kind regards

  22. laura says:

    Mr Woodford – I wondered if I could seek your views on using Goat Milk Formula instead of Cow milk formula (as mentioned in great detail above by another commentator). Do you know if goats milk has casein?

    • Keith Woodford says:

      Yes, goats milk contains casein. The beta-casein is of the A2 type as in A2 cow milk.
      That is probably a key reason why the goat formula is popular, although most users will not understand it is the beta-casein that is making the difference.
      Keith Woodford

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