New findings published by Nature Research, demonstrating how A1 milk predisposes for asthma and lung inflammation, should bring the A1 milk issue back into focus for both consumers and farmers

New findings published by Nature Research, demonstrating how A1 milk predisposes for asthma and lung inflammation, should bring the A1 milk issue back into focus for both consumers and farmers

Until May 15 of this year, there had been a lack of new scientific evidence about A1 milk for almost a year. The reason it was quiet is because no-one had been funding the next studies that needed to be undertaken. However, new evidence has now come forward from India, somewhat out of left field.

Prior to this, there had been multiple strands of evidence demonstrating that A1 beta-casein and hence A1 milk is pro-inflammatory and linked to auto-immune conditions. However, the new research published by Nature Research in the journal ‘Scientific Reports’ is the first to explore these pro-inflammatory and immune-related effects of A1 beta-casein in the airway and lungs.

For those new to the A1 versus A2 milk issue, or needing a refresher course, the A1 versus A2 milk issue relates to whether or not the beta-casein in the milk is of the A1 or the A2 type. A lot of milk from European breeds of cows is of the A1 type whereas Asian cattle, sheep, goats, all humans and many other species of animal produce milk where the beta-casein is exclusively of the A2 type. The A1 milk, when digested, releases a protein fragment called beta-casomorphin which has opioid characteristics. This opioid can have a myriad of effects.

As to why the funding of A1 beta-casein science has gone a little quiet recently, the answers are that it is a consequence of global dairy-industry politics and commercial positioning. That is a story for another time. However, in the meantime most of the big international dairy companies have been positioning themselves with A2 product offerings, particularly in the infant-formula category. Infant formula is the most profitable dairy category for those who manage to get a foothold in a very crowded field.

Anyone who follows the stock exchange will know that ‘The a2 Milk Company’, which is the New Zealand registered but dominant global company in the A2 category, has grown to have a market capitalisation more than twice that of Fonterra. It has been a huge success, based on original science undertaken in New Zealand, but with most of the company now owned by overseas investors. Oh dear!

The science journey started with investigations by Professor Bob Elliott, who has in recent days been awarded a knighthood in the latest Queen’s Birthday Honours. It was Elliott, now ‘Professor Sir Robert Elliott’ who identified A1 milk as a risk factor for Type 1 diabetes.  From there, the A1 versus A2 beta-casein research spread into many other health fields.

 Returning here to the latest research, the paper published by Nature Research investigates whether prolonged use of A1 milk predisposes for asthma and other lung conditions through breathing-passage constriction and pro-inflammatory effects. The short answer is that it does, and the evidence is powerful with high statistical significance.

There is a lot of health research, particularly relating to foodstuffs, where it is extremely difficult to conduct the research directly in humans. That is a key reason why nutrition research is typically controversial and contested. Results often take a long time to show up, which makes clinical trials exceedingly difficult, even if ethics approval is granted.

For many trials, ethics approval is impossible. So, for cause and effect questions that need proof and not just epidemiological correlations, the work is often done with animals.

In this case, the research was done with mice that were fed the equivalent of one glass of milk per day for thirty weeks (210 days), with this being squirted down their throats.  Then the mice were treated with methacholine which is a standard method in humans for testing whether someone is susceptible to asthma. At that point the mice had to make the supreme sacrifice so that all the measurements could be taken.

Of course, if this research had been undertaken with only A1 milk, then it would have proved nothing. Other groups of mice, all housed individually, were fed either A2 milk, or a 1:1 ratio of A1 and A2 milk. There was also a control group that were drenched with distilled water.

The results were very clear. The mice that had been on a diet of A1 milk were much more susceptible to asthma when dosed with methacholine. This was caused through both airway constriction and inflammation in the lungs.

The mechanism behind the result was also very clear, being what scientists call Th-2 driven. This means that the immune system becomes unbalanced and there is overproduction of cytokines such that the body is damaged by its own actions.  Specific cytokines that were over-produced include interleukin-4 and interleukin-5.

The term ‘cytokine’ is well known to immunologists but has only recently entered the general lexicon, largely through its association with COVID-19. When people die suddenly from COVID-19, it is typically from a cytokine storm which leads to organ failure through lack of oxygen. Coincidentally or not, the mechanism is essentially the same – an immune over-reaction leading to excessive cytokine production.

The evidence from the current study is that the A1 milk itself is not the final trigger. Rather, long-term exposure to A1 beta-casein creates an immune environment more susceptible when the trigger gets pulled by some other factor, in this case methacholine. Conversely, in the absence of A1 beta-casein, the trigger, which can be either be a specific foodstuff or a virus, is much more likely to either fire a blank or a low-powered half-shot.   

With humans, the susceptibility to various diseases including asthma and pneumonia-type conditions varies between individuals. This is because of genetic variation between individuals. Some people have weak immune systems, others have overactive immune systems in response to specific situations.  However, all humans have the same Th-2 and cytokine driven immune systems. It is the sensitivity that varies between individuals.

With the specially inbred mice, all were similarly susceptible to specific environmental conditions and triggers. This is what made them a good animal model to test out the Th-2 and cytokine driven mechanism, in this case set-up by the A1-milk environment.

With hindsight, the results should come as no surprise.  It was already known both for humans and animals that A1 beta-casein is pro-inflammatory through these same Th-2 and cytokine mechanisms. It was just that no-one had done a trial to prove it in relation to asthma and the lungs.

When trying to evaluate the credibility of a study, most people ask several questions. Are the results statistically significant? Is there evidence for the mechanism?  Is the mechanism plausible for humans?  Who published the study? Who authored the study and did they have conflicts of interest?

The first three questions have already been answered as a strong ‘yes’. The fourth question has also been answered – the study was published by pre-eminent Nature Research. The answer to the fifth question is that the six authors are scientists employed by various governmental research institutes and universities in India, and they all declared that they had no competing interests. India has considerable interest in A2 milk because their native cattle are A2.

For those who want to dig deeper, the article is open access at  Here is the full link.   A gentle warning is that the paper does assume some prior knowledge of immunology.

*Keith Woodford is a retired professor from Lincoln University (NZ) and retains an honorary position there as Professor of Agri Food Systems. As one element of broad-ranging scientific interests, he has been writing about A1 and A2 beta-casein for many years. This includes a book ‘Devil in the Milk’ on the science and politics of the issue, first published in 2007 in NZ, and with subsequent American and Russian editions. More recently he has co-authored five research papers with medical colleagues in international nutrition and medical journals on further research into A1 and A2 beta-casein. Articles for non-scientists are archived here.

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Fonterra could have purchased A2M for peanuts back in the day now they have to partner with them funny how things turnout.

I do recall a discussion with a Fonterra director who once said to me, with an element of condecension, that Fonterra could buy out A2 Milk for $50 million if it wished to do so at any time. That was in about 2009 or 2010. The market value now is close to 300 times that figure. And a buyout would need to be pitched at around $20 billion or maybe more. Fonterra could still make a lot of money from A2 products but only if they developed their own international brands. Instead they have chosen to be an ingredient supplier to 'The a2 Millk Company'. That arrangement was a great deal for The a2 Millk Company as it took their key potential competitor out of the market. Given Fonterra 's current mindset, having been bruised so badly in recent years, they could as an alternative have also made significant money if they were to sell A2 products themselves on the ingredient market to allcomers. But it seemeed simpler to tie themselves to The a2 Milk Company.

Any reason why comments were deleted thanks editor

I can see that my comment about the possibility of removing the opioids from A1 milk was deleted. I have done a bit of digging around the internet to find out if the opioids could be extracted and also just how addictive they may be. So far it appears that tests on rats have shown ingestion of milk products containing β-casomorphin is not likely to become the focus of an addiction.

β-Casomorphin does sound interesting however:

β-Casomorphins are resistant to the action of gastrointestinal enzymes (Read et al., 1990) and have been associated with the following activities: antihypertensive, immuno-modulatory, antidepressant, antisecretory, and antidiarrheal activities (Pihlanto, 2001). Opioid peptides are thought to be biologically very potent; potentially, micromolar amounts may be sufficient to exert physiological effects (Meisel and Fitzgerald, 2000).

Perhaps this quality of A1 milk will make it more attractive to consumers which is something Woodford doesn't want hence the deletion.

I have no idea why your comment was deleted - I do not control that.
No, it is not possible to remove the beta-casomorphin from A1 beta-casein as it is embedded within the protein and only releaed on digestion.
Yes, there is evidence that beta-casomorphin is addictive but that is not the most important issue. The other health issues are more important.

Hopefully Mr Muller wasn't with Fonterra during the time they were laughing at A2 milk...who's laughing now.
Little known fact is MP David Parker was once involved with A2;
'He fell back on law to keep "the dogs at bay", and before long found far more success in the agri-tech finance world with Blis Technologies, where he could bring together his love of science and business. He soon joined Howard Paterson, then the richest man in the South Island, at A2 Milk, a company now worth a whopping $9 billion. '

Since that extract above,A2 has surged even more,worth approx 13.86b and likely to enter the ASX50 at the next rebalance in June.

Muller would have been there for part of that time but with no involvement in A2 strategy.
None of the directors had any empathy for A2 until Nicola Shadbolt came on board. From memory that was 2009. Nicola had been breeding to A2 from well before that. However, John Wilson was always negative to A2 and so was John Monaghan in those days. Theo Spierings claims to have seen merit in A2 by around 2013 or 2014 but I don't think he put much if any energy into convincing the Board at that time. However, the decision to link with A2 in early 2018 was definitely a Theo move. However, I think the specifics of the agreement that he and one other Fonterra executive drew up with A2 were greatly flawed.
Yes, David Parker was holding the reins at A2 Milk when Howard Paterson and Corrie McLachlan were originally getting the show on the road.

Thanks Keith,you are a wealth of knowledge on A2 and a flag bearer from way back.

I would question "The answer to the fifth question is that the six authors are scientists employed by various governmental research institutes and universities in India, and they all declared that they had no competing interests." The competing interest is the Country

A competing interest is normally defined as a relationship, not otherwise apparent, that could lead to a perception that the authors stand to benefit financially from the authorship. So the authors are saying that they have no financial association with the dairy industry. Their country of domicile is already evident so is not stated again, and yes, they do have to come from somewhere.
The issue of A1 v A2 is somewhat controversial in India with the large commerical herds (taurus breeds) having considerable proportion of A1 in the milk they produce, and the small farmers in many cases having local breeds (indicus rather than taurus) which produce less but are heat tolerant and produce A2 milk.

Thanks. I'm aware of the usual context of conflict of interest definition but ramped this up to a higher level of country gaining financially. Unaware of the fact that there is also A1 milk produced so now conflict of interest is more relevant to the individuals not having an A2 interest. The proportion of A1 to A2 in India could also have some bearing on the situation. You might like to elaborate on that. In addition India is typical of most Asian countries on a corruption level and hopefully this doesn't extend to academia.

Unfortunately science is riddled with corruption, in most if not all parts of the world.
If you read my book 'Devil in the Milk', you will see that I wrote about some of that corruption, which was in Western countries and involved the hiding of data that would have exposed the health issues with A1. When I get around to writing the next edition of the book - there is now so such more to write - I will have more to say on the role of commerical entities who hid key information. When I wrote the first edition, my publisher was very brave to allow me to say what I did, as he carried no insurance for any subsequent court cases. All he required of me was to tell the perpetrators of withheld evidence that we were withthholding one piece of evidence, that if we were sued, we would bring out in any court case.
Keith W

Keith, I can never understand how the oils supplanted butter in our food e.g. baking, sandwiches, toast, etc, etc.
My mother is still going strong at 96-years-old and has butter everyday not to mention ice cream every evening for pudding. And I do too as I am one of those rare individuals whose digestive system cannot tolerate oils of any description e.g. canola, olive, name it! (I've only ever come across 2 or 3 others who have the same problem). I can't eat the oil-filled biscuits or cakes 'off the shelf' with the exception of butter shortbread. Most of the scones today are also made with oil.
It's been said that the advent of the dominance of oils in cooking came about because of the successful marketing done by the oil manufacturers on the one hand or because of the supposed deleterious health effects of butter. My mother's survival to 96 years on a butter diet would seem to be living proof against the latter.
Or could it just boil down to the fact the oils are cheaper than butter? Or maybe it's a combination of all the above.
Could you please give me your take on this situation.

I really have no clear idea on that issue. The oils you mention contain both saturated and unsaturated fatty acids. My suspicion is that your intolerance is to phenol compounds within these oils rather than the fats themselves and this will be linked to the absence of a specific enzyme in your digestive system. Are these the only foods you have problems with?
Keith W

Conclusion..drinking milk causes high cases of asthma and inflammation.

Correction,drinking milk containing A1 causes high cases of asthma...

"The prevalence of overweight and obesity has escalated dramatically during the last decades both in children and adults. This recent epidemic is not attributable to genetic factors as it occurred over a short period
where substantial changes in population gene pools cannot be seen. Among environmental factors, physical
inactivity associated to increased caloric intake, i.e. in practice to high-fat diets, plays an important role.
However, in addition to a positive energy balance, our results pointed out the antithetic properties of polyunsaturated fatty acids of the n6 and n3 series [57] in promoting mouse adipose tissue development.
The data indicate a significant increase in the n6 PUFA content and in
the LA/LNA ratio of breast milk, formula milk (except in the last 10 years for the LA/LNA ratio) and
most consumed foods over the last decades. It should be stressed that changes in the lipid chain processed,
foods and human food habits have taken place rather smoothly and that it is difficult to relate these alterations at a precise time where obesity epidemics began to ‘‘explode’’. "

Recent evidence suggests that consumption of whole fat dairy products may, in fact, be protective against obesity

Just be sure that it's A2 whole fat dairy. I've been reading Keith's book The Devil In The Milk lately, very interesting. It lays out many of the potential problems with A1 milk while admitting there may be benefits which counter-balance the negative effects to some extent. The argument (as far as I have read so far) isn't that A1 milk is necessarily bad for you, but that A2 milk gives you all the same benefits without the negatives. Hence the huge success of the A2 Milk Company I guess.

Zachary et al
A balanced diet includes both fat and carbohydrates, and the fats need to include all of saturated, mono-unsaturated and poly-unsaturated. Too much saturated fat is strongly implicated in heart disease. Zero saturated fat will lead to poor brain function among other things. A diet based predominantly on carbohydrates can lead to obseity because many carbohydarates, including sugars, metabolise quickly and leave the person hungry again after a short while. Fats take longer to digest and therefore hunger cravings take longer to return. However, a diet with no carbohydates creates its own problems because it forces to fats to be metabolised by a different process and this can lead to ketosis, which can be recognised by distinctive smelling breath. Ketosis is not a good state to be in.

Myth 1: Milk builds strong bones.

The dairy and bone health link is one of the most pervasive milk myths. One large-scale Harvard study followed 72,000 women for two decades and found no evidence that drinking milk can prevent bone fractures or osteoporosis. Another study of more than 96,000 people found that the more milk men consumed as teenagers, the more bone fractures they experience as adults. Similarly, another study found that adolescent girls who consumed the most calcium, mostly in the form of dairy products, were at greater risk for stress fractures than those consuming less calcium.

I find that very hard to believe. Poor Asian diets led to some very short people. But that is changing with western diets and milk products

It is lack of protein that has led to many Asian people being short in the past. And milk does solve the problem.
But it is also correct that drinking milk does not lead to strong bones.
That myth has been widely exposed in most parts of the world but still seems to live on in NZ. The way to build strong bones is to have exercise, particularly when young, and have exposure to UV light, which leads to synthesis of vitamin D.
Calcium supplementation has very much gone out of favour in most parts of the world.
However, it is true that if people get no milk or eat insufficient greens then they can get rickets.
When people talk about calcium from milk, I sometimes ask them where do they think the cows gets their calcium from. The answer is that it comes from the green grass.