It is always exciting to encounter a fresh topic that has escaped attention, yet with a little investigation, demands it. So it is with the story of A1 / A2 milk. I first became aware of the existence of this issue at a potluck dinner with health-conscious fellow diners. As it turns out, this is old news to residents of New Zealand, where a few researchers and entrepreneurs have been promoting the virtues of A2 milk for about a decade. The story is about the role of a milk protein, beta-casein, that can take on two very similar forms, called A1 and A2, depending upon a single simple mutation of one gene. The A1 form of the beta-casein, upon digestion, breaks down into beta-casomorphin-7 (BCM7), a fairly stable and strong opiate which appears to cause health problems in some people some of the time. Meanwhile, the A2 beta casein proteins are digested completely and don’t generate the problematic BCM7.
The evidence suggests that BCM7 can trigger the auto-immune response responsible for Type 1 diabetes, and it is implicated in arterial damage and consequently could be a factor in heart disease. In addition, there is evidence for connections between BCM7 and autism, schizophrenia, sudden infant death syndrome (SIDS) and milk intolerance.
The story is well-told by Keith Woodford in his book, Devil in the Milk: Illness, Health and the Politics of A1 and A2 Milk. The author has a nice synopsis of the major scientific findings on his website. I find the evidence and the arguments he presents for the case against A1 milk quite compelling. But what makes this story particularly interesting, and the book fascinating reading, are the personalities that have shaped policy surrounding the science and the agriculture, and the all-too-predictable response of large organizations against making any kind of change.
The solution to the A1 milk problem is easy. Just stop breeding dairy cows using bulls with A1 genes, and in a few cow generations the milk will have a lot less A1 beta casein in it. The cost for such an adjustment is minimal. Many of the dairy bulls used for artificial insemination have already been genetically tested and their A1/A2 status is known. The cost of genetic A1/A2 testing is only a few dollars per head; nothing compared to the cost of raising breeding stock.
But we live in a world where brand is everything. Any hint that milk might not be the most wholesome of foods just cannot be allowed to reach the public. In New Zealand, where this issue first became known, the large milk marketing company Fonterra was always ready to downplay and counter any scientific findings that hit the public media. The milk companies and government regulators have been content to let reasonable scientific skepticism serve as an excuse for doing nothing, and presently this is the state of affairs.
Let’s look at just a bit of the evidence for the A2 milk hypothesis, just to give readers a glimpse of the argument and potential health consequences. We will look at the results from a study by Murray Laugesen and Robert Elliott, published in Journal of the New Zealand Medical Association in 2003. The graph below shows the death rate from ischemic heart disease as a function of A1 beta-casein consumption for several countries that all have established health care systems. The trend is obvious and is highly unlikely to be due to chance.
The authors look at other correlations, such as total milk protein, butter fat, or other dietary differences, but nothing has as strong a correlation as A1 beta-casein consumption. The study also looked at the correlation of A1 beta-casein consumption with the incidence of Type 1 diabetes, and here the correlation was even stronger.
If you take the study numbers at face value, and assume that, in the US, the milk supply could become free of A1 beta-casein, then you might expect a reduction of about 40 deaths per 100,000 annually due to heart disease, just extrapolating from the linear correlation coefficient in the chart above. This would amount to about 60,000 fewer deaths from heart disease every year. (For perspective, auto accidents kill about half that number.)
Scientific “proof” that there is a problem with A1 beta casein is a standard that will not be reached until long-term double-blind studies are done on humans – which could be decades in the future, if ever. The cost of such studies could easily be more than the cost of just solving the problem! That the solution is so simple with such low costs, the down-side risks virtually nonexistent, and the potential public health benefits so large, make this issue a fascinating case study in the politics of indecision.
The best solution would be for some industry group or public entity to promote or require farmers in a defined geographic area to begin the switch to only A2 milk-producing cows. In the matter of a few years, with good record-keeping and now with a significant sample size, the change in A1 beta-casein content in the milk supply should show up in a change in the incidence of Type 1 diabetes and heart disease statistics.
Individually, the risks from milk are not high, just as riding in a car is not particularly dangerous. However, if the driver is drunk, or the body is prone to other compromises, even individual risks can become significant. In the US, the only source of milk that does not contain A1 beta-casein is goat milk, or milk from cows that are known to be genetically A2A2 homozygous individuals — difficult if not impossible to find. In other parts of the world, A2 milk is becoming more available.
I suspect that someday there will be no more A1 beta casein allowed in milk, but that time is a long time away. In the mean time, don’t expect our health watch-dogs to protect you any better than they did from cigarette smoking.