To skeptics, the public-health campaign looked like a money grab.
Seventeen years later, this war of competing interests has only intensified. As biased polemics continue to muddy the waters of the research surrounding the discovery, A2MC has managed to secure some 12 percent of the Australian dairy market. They have entered markets in China and western Europe, and predict a full U.S. rollout by 2018.
While American commodity farmers have been every bit as territorial as their Australian counterparts, some small farms have begun converting their herds over the past few years, sliding A2 genetics into their portfolio of value-adding concepts like grass-fed and local. At a time when American grocery stores stock far more varieties of plant-based or otherwise specialty milk than they do commercial cow’s milk, these small-scale farmers have a built-in receptive audience.
Now, A2 milk stands poised to take these niche markets by storm—but first American consumers will have to be convinced that it’s actually good for them.
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The split between A1 and A2 milk was discovered about 25 years ago in milk’s most abundant protein, beta-casein. The variation occurs in the protein’s chain of 209 amino acids: A1 has the amino acid histidine at position 67 in the chain, while A2 has proline there instead.
Despite its name, A2 is actually the original variety. Historians believe that the A1 mutation originated in Europe somewhere around 8,000 years ago, but why it occurred is open to speculation. Some believe that farmers began breeding for higher output at this time, and favored the A1-dominant breeds like Holsteins known for producing more milk. Others speculate that the mutation was caused by forces more cosmetic than substantive; Holsteins are the classic black-and-white cows that dot pastures throughout the western world.
“It could have been something as simple as the first cow to have a black-and-white color by chance also carried the A1 version of the gene, and farmers then said, “we like the look of these,” said Keith Woodford, an honorary professor of farm management and agribusiness at New Zealand’s Lincoln University. A2-dominant breeds wound up in Asian and African countries, possibly because they were less in-demand and relegated to cultures that consumed less milk.
McLachlan and Elliot’s big discovery back in 1993 was that A1 produces an opioid called beta-casomorphin, or BCM-7, when it hits the small intestine. A2MC’s studies have gone on to claim that BCM-7 causes inflammation that leads to myriad health issues, ranging from eczema and indigestion to diabetes, schizophrenia, and autism.
In 2007, Woodford published a book about the dangers of A1, Devil in the Milk: Illness, Health and the Politics of A1 and A2 Milk, which boosted A2 milk sales and prompted the New Zealand Food Safety Authority and European Food Safety Authority to propose rigorous analysis of A2MC’s health claims. The EFSA’s report, issued in 2009, rejected most of the evidence. It found that in “most if not all” animal studies prior to its publication, scientists had injected BCM-7 directly into their animal test subjects, rather than administering it orally, which in the EFSA’s view rendered the results irrelevant to human consumption. The review also chastised McLachlan and Elliott for being too quick to link the prevalence of chronic disease in a country to the abundance of A1 cows in that country, when disease could also be explained by factors environmental, political, or cultural. In other words, correlation does not equal causation.