Is A2 milk going to make us healthy?

Around the world, A2 milk is being sold. Due to its market launch in The Netherlands, I decided to take a closer look at the product, and the science behind it. But before going into the details, first I want to explain what A2 milk is. Milk contains 6 major proteins, 4 caseins (that are the basis of cheese making) and 2 whey proteins (that remain in the whey after cheese making). One of these four caseins is β-casein, which is also the second most abundant protein in milk. This β-casein has an amino acid composition that depends on a gene, that can have small variations. The two main version are A1 and A2, which differ by one amino acid. During breakdown of β-casein, this can lead to the formation of a peptide called BCM-7.

Primaeval cow

In the Netherlands, the milk is marketed as coming from primaeval cows. Also in other countries, marketing focuses on the fact that A2 is the original β-casein, and A1 is the version that comes in our current milk due to breeding. This is simply not true. In all kind of cow breeds other than the regular Holstein cows, A1 and A2 can both be found. Between breeds, there is a difference in the ratio of the A1 and A2 gene. But A1 can be found in all cow breeds, not only modern breeds. On top of that, for the Dutch Friesean Holstein breed (most popular dairy breed in the Netherlands) actually at least 70% has the A2 gene for β-casein. And due to the positive association between A2 and protein yield, breeding programs will probably increase A2 further in future. Not because they believe it is healthy, but simply for economic reasons.

BCM-7 and chronic disease

In the 1990’s and early 2000’s, a lot of attention was on the potential link between BCM-7 and chronic disease. Originally, this was based on epidemiological studies, but on further investigations, these were not reliable to assess the relation between β-casein and chronic disease risk. In animal models where BCM-7 is directly injected in the blood stream, negative effects were shown. But trials in humans eating caseins have never been able to show this happens in people. The most probable reasons for this is that BCM-7 can be, and therefore probably is, further broken down in our intestinal tract. This has been confirmed in a 2009 EFSA report, which came to the conclusion that A1/A2 is not plausibly related to chronic diseases.

A1/A2 casein and cow’s milk allergy

A lot of farms selling A2 milk directly to consumers focus on cow’s milk allergy. I’ll be short on this one. Because 1) hardly any person with cow’s milk allergy is allergic to β-casein alone, and 2) only one amino acid is changed, I don’t expect any cow’s milk allergic person to benefit from A2 milk. And for the people who claim it helps, I have never seen evidence in double blind provocations, but always based on self-diagnosis, which is known to be very unreliable in food allergy in general.

A1/A2 casein and intestinal discomfort

Recently, a new hypothesis has popped up, the β-casein variant may be related to intestinal discomfort. This is a difficult to categorize “illness” (if you can call it an illness), so very popular for healthy products that can’t make strong claims. Intestinal discomfort may be from lactose intolerance, but in that case A2 milk won’t help. Then there are the people with undiagnosed weak symptoms (among whom gluten-free products are also popular). A recent study on 45 Chinese people, they showed a small decrease in intestinal discomfort after consuming A2 milk for 2 weeks. I’ll be a bit careful on this one. Many small-scale (low number of participants, short intervention) nutrition studies can’t be replicated, so we’ll need to see how that goes with this study. Also, we don’t know whether, even if replicated, Europeans (where lactose intolerance is less common) would respond the same. So we’ll just have to wait for further proof. In conclusion, for the time being, I don’t see any reason, for anyone, to already consume A2 milk.

This blog is based on two blogs I earlier wrote in Dutch for the The Milk Story

Kasper Hettinga, October 2016


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