A1 vs. A2 Milk

Large scale epidemiological studies have linked casein (a cow’s milk protein) to autoimmune disease and heart disease (see The China Study).  I just ran across the following twist on this theme which purports to explain a mechanism: a genetic mutation many years ago in domesticated cows transformed the original, safe casein (“A2”) into a toxic form (“A1”).  Most cow’s milk available today has both.

What do people think of this?  Has anyone tried personally to ingest milk products that are exclusively A2?

Given the dubious connection between cholesterol and heart disease, could the bad rap on cheeses, cream and ice cream have more to do with A1 and sugar than the animal fat and cholesterol?

  • Anonymous

    I think your premise is flawed. The China Study doesn’t demonstrate significant adverse effects from dairy in humans. See:

    http://rawfoodsos.com/2010/06/20/a-closer-look-at-the-china-study-dairy-and-disease/

    It does show a casein link in rats when they consume massive quantities. But not when they consume moderate quantities.

    • Rafe Furst

      The book “The China Study” draws from a much larger dataset than just the specific eponymous study. It gives evidence that casein is implicated in autoimmune disease and cancer. Assuming the argument is not flawed, then perhaps the A1 vs A2 provides a causal mechanism.

    • Rafe Furst

      The book “The China Study” draws from a much larger dataset than just the specific eponymous study. It gives evidence that casein is implicated in autoimmune disease and cancer. Assuming the argument is not flawed, then perhaps the A1 vs A2 provides a causal mechanism.

    • Rafe Furst

      The book “The China Study” draws from a much larger dataset than just the specific eponymous study. It gives evidence that casein is implicated in autoimmune disease and cancer. Assuming the argument is not flawed, then perhaps the A1 vs A2 provides a causal mechanism.

      • Anonymous

        That Web site thoroughly demolishes the entire evidentiary edifice of the book, not just the the original monograph. See for instance comments on other papers cited:

        http://rawfoodsos.com/2010/08/06/final-china-study-response-html/#sec2

        Looking for a causal mechanism for a correlation that doesn’t exist is fraught with all sorts of logical pitfalls.

        I’d focus more on the the A1/A2 specific research which appears to be confined primarily to Type 1 diabetes, with some evidence for a role in IHD. It certainly seems plausible that some people may have heightened immunosensitivity to particular proteins. You’d think you could do a blood assay to measure different people’s reactions to A1 and A2 to figure this out pretty quickly.

        • Rafe Furst

          The larger point (which the China Study may or may not have bearing on) is that the most credible and definitive epidemiological studies (a) contradict one another (b) contradict “known” etiology and (c) have dubious value for individual human choices. Once I’ve laid out various aspects of these practical dilemmas, I’ll tie it together with an argument as to why this might be the case not only in practice, but in theory as well.

  • Dave Lambert

    Another flaw in the casein analysis, or food analysis in general, is that the overall health effects of a particular food is a sum of all of its parts, not just the effect of an isolated component.

    For example, their are two types of protein in milk: casein and whey. Numerous studies have shown that whey is likely a strong cancer preventer. Thus, even if casein does cause cancer when isolated on its own, it could still be the case that milk is a net cancer preventer.

    • Rafe Furst

      I couldn’t agree more. I also suspect that we can’t take a particular food in isolation either. It is consumed at a particular moment along with other foods that affect bioavailability of micronutrients for one thing. Total diet has to matter too. Plus epidemiological data suggests social context of meals affects mortality and morbidity. The list goes on.

      My tentative conclusion is that discussing an isolated compound is meaningless at best and guaranteed to obfuscate much more important aspects of reality.

  • Pingback: Epidemiology vs. Etiology - The Emergent Fool()