Milk May Endanger Your Health, and the Dairy Industry Knows It

A mutant protein has invaded the world's dairy supply, including, most likely, the milk in your fridge.

The protein, called A1 beta-casein, is well known in the scientific community. While most dairy companies, trade groups and government agencies consider it harmless, a growing body of research implicates A1 beta-casein in diabetes, heart disease, autism and schizophrenia.

The original mutation occurred several thousand years ago, causing cow zero and its offspring to produce milk in which the amino acid histidine occupies the 67th position of the beta-casein protein found in milk solids.

The amino acid proline occupies that position in the nonmutant, original form of the A2 protein. Today, the average vessel of milk contains milk from many cows, with a mixture of both A1 and A2 beta-casein.

Keith Woodford, a professor of farm management and agribusiness at Lincoln University in Christchurch, New Zealand, is spreading the word about what he believes to be the dangers of milk containing A1 beta-casein.

His book, Devil in the Milk, builds on more than 100 peer-reviewed studies to present a compelling case that A1 milk poses substantial health risks.

The book is a technical read, and conspiracy theorists will find it gripping, as Woodford details the extent to which corporations and government bodies with entrenched interests in maintaining A1 milk's reputation have disputed, ignored and silenced evidence suggesting there might be a problem.

If Woodford is right, those fighting to sweep this research under the rug are endangering the health of millions, if not billions, and for little in the way of return. He says it would be a simple matter to remove A1 beta-casein from the word's milk supply.

A New Zealand company, A2 Corp., has patented means of testing cattle for the A1 mutation. The company assists dairies in switching their herds to A2 production, which takes about two generations, or 10 years. A2 Corp. also certifies dairies that produce pure A2 milk and helps market it.

While Woodford makes it clear neither he nor his family have any financial interest in A2 Corp., it's clear he hopes the company succeeds.

Countries with the highest levels of A1 in their milk also have the greatest incidence of Type 1 diabetes and heart disease, Woodford explains. This observation inspired a study on rodents, in which one group of rats was fed A1 beta-casein and the other was fed A2. None of the A2 group developed diabetes, while half the A1 group did. Other animal studies implicate A1 in heart disease.

The evidence linking A1 milk to autism and schizophrenia follows similar lines: Correlations in population studies and support from animal studies, but scarce research on human subjects.

Direct research on humans, Woodford explains, is fraught with ethical and practical difficulties:

The subjects of the trial would need to be identified as babies and then put on either A1 or A2 formula milk once breastfeeding ceased. The trials would probably need to go on for many years, and the children prevented from eating any "ordinary" dairy products. The parents of each child would need to give permission and be actively involved, but could not be permitted to know whether their beautiful and initially healthy baby was getting the A1 or A2 formula.

The theories for how these maladies might manifest from A1 milk and not A2 center on a protein fragment known as BCM-7, which is released when A1 beta-casein is digested. BCM-7 is found in high concentrations in the urine of autistics and schizophrenics.

As for the connection to diabetes, Woodford suggests that since BCM-7 is similar to an amino acid sequence in the insulin-producing cells of the pancreas, the body might mistakenly attack these cells in an effort to get rid of BCM-7.

The lack of direct proof of a link between A1 milk and any diseases -- which only human trials could produce -- has been latched onto by the A1 defenders.

There's "not sufficient evidence for the claims being made by the marketers of A2 milk," I was told, via e-mail, by the National Dairy Council's Stacey Stevens. "Reviews of the science to date confirm there's no reason to think A2 milk might have health benefits beyond those of regular milk."

This statement seems to dodge the fact that the issue I had asked her about isn't the supposed health benefits of A2 milk, but the possible health risks of A1 milk.

Stevens responded to my initial query promptly, but I received no response when I asked her to clarify the Dairy Council's position by agreeing to the statement, "There is no reason to think that A1 milk might have health risks."

Stevens' response is typical from the dairy industry. Woodford thinks it's a result of fear that the public will get scared off all milk.

"We're comfortable that all milk -- A1 milk, A2 milk -- is really good for you, and you should keep drinking it," said Carole Inkster of the New Zealand Food Safety Authority in a New Zealand television report on A2 milk. Fred Brenmuhl, of New Zealand Federated Farmers responded to the potential dangers of A1 milk by saying, "Stopping the consumption of milk products is probably more dangerous than anything else."

In May 2007, A2 Corp. began marketing A2 milk in the U.S. produced by Prairieland Dairy in Nebraska. But in December 2008, the company temporarily discontinued its U.S. marketing efforts in order to rebrand and relaunch A2 milk products more broadly.

In the meantime, if you wish to avoid A1 beta-casein, you have a few options: Milk from goats and sheep doesn't contain A1 beta-casein.

Dairy products made from milk fat, like butter, don't contain A1 beta-casein, even if the milk they were made from did. The jury is still out on the A1 content of cheese and yogurt.

Beyond the one-time expense and inconvenience of switching their herds, Woodford says there is little for the dairy industry to fear in the possibility that A2 milk is safer, and he regrets the industry continues to view the issue as more of a risk than opportunity.

Although frustrated, he isn't completely surprised, even at resistance from within the scientific community. He cites many examples of slow acceptance of new medical ideas, including Robin Warren's 1979 discovery that stomach ulcers are caused by bacteria.

Warren received the Nobel Prize in 2005, Woodford writes, but in 2000 "the work was still being described as 'controversial.' "

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