In the late 1990s, a group of researchers published studies that sent a shockwave through the nutritional industry. The research apparently indicated that a molecule called beta-CM-7, which results from the breakdown of milk in the colon, could cause autism, juvenile diabetes, allergies, schizophrenia, Parkinson’s disease and heart disease (McLachlan 2001, Elliott et al. 1999, Laugesen and Elliott 2003) .
These researchers also happened to be armed with the alternative: A2 milk. The culprit theoretically was beta-casomorphin-7 (beta-CM-7), which was found in higher quantities in some milks than others: Notably from cows (appropriately called A1 cows) from Northern European countries, North America and Southern Australia. As the story goes, countries that so happened to have more A1 cows and A1 milks, also suffered from with higher rates of those diseases mentioned above.
As the theory goes, the case against A1 milk is based upon a seeming mutation that occurred somewhere between 5,000 and 10,000 years ago, apparently at the point when cows were being domesticated in Europe. This produced what is now called the A1 breed of cow and cow’s milk. A2 cows, according to the hypothesis, have not undergone this mutation.
A2 cows supposedly include some Guernsey and Jersey cows. Most Asian and African cows are supposedly also A2 cows. In addition, goats, yaks and sheep theoretically produce A2 milk. Holsteins, for example, and most other commercial breeds of cows in the U.S., apparently produce primarily A1 milk.
The A1 vs A2 milk controversy has raged over the past few years. Apparently, it is the beta-casein protein that is the cause of concern. Beta casein contains 229 amino acids, of which proline lies at the 67th position in A2 cows, and A1 cows produce beta casein with a histidine-converted amino acid at this position.
The hypothesis claims that the proline amino acid within the A2 beta casein will strongly bond to this protein called beta-CM-7. This supposedly prevents its release, where as in the case of the histidine beta casein from the A1 cows, the beta-CM-7 will be released within the gut when the A1 milk is consumed.
All of this said, there is good reason to believe that the A2 milk hypothesis is unfounded. For example, the New Zealand Food Safety Authority commissioned a study in 2004 to investigate the claims. The review, led by Professor Boyd Swinburn from Melbourne Australia’s Deakin University, concluded little evidence that A1 milk produced an increased risk of disease.
In addition, in 2009 the European Food Safety Authority (EFSA) reviewed the evidence on A1 and A2 milk, and they also could not establish a relationship between A1 milk proteins and increased disease.
The very interesting thing about all this is that it is not all about the science. There are are corporate interests with profit motives involved. More specifically, the A2 Corporation holds a patent on the testing for beta-CM-7. It also holds a strangle-hold on the conversion of A1 herds to A2 herds, through the artificial insemination of a A2A2 bull, sold by, yes, the A2 Corporation.
A critical question that this brings up is how can independent researchers verify the hypotheses that certain cows are A1 and others are A2 if the test cannot be conducted outside of the A2 Corporation’s patent? This seeming conflict of the patent (along with other issues about the A2 milk research) was highlighted in a critical review published by the European Journal of Clinical Nutrition in 2005.
It should be understood that autism, diabetes, neurological diseases and heart disease are traceable to a number of associations. There are many, even multiple associations possible among these diseases, from diet to genetics to air pollution to nutrients to toxins to sunlight.
In fact, much of the A2 research grounds itself on epidemiological research associating previously unrelated elements of these disease rates and the primary genetic makeup of milk herds among those countries.
Curiously, these same countries that supposedly have higher levels of A2 milk are also known for other things, including a higher consumption of animal products in general, higher levels of toxins, colder weather and less sunshine.
New Zealand’s University of Otago biochemistry researcher Dr. T.R. Merriman (2009) has pointed out that these “A1 countries” are specifically associated with geographical latitude. He illustrates that a number of studies have associated those countries further away from the equator with greater incidence of type-1 diabetes, for example. Dr. Merriman also illustrates that significant research illustrates that type-1 diabetes is associated with lower levels of vitamin D (a product of sunshine). This data, as Dr. Merriman puts it, “convincingly implicate vitamin D deficiency in T1D [type-1 diabetes].”
In addition, a number of studies have now linked schizophrenia, Parkinson’s disease and other neurological conditions with vitamin D deficiency. In a recent review done by French neurological researchers (Annweiler et al. 2010), 127 studies confirmed an association between these disorders and vitamin D deficiency. They concluded that, “Vitamin D has been associated with many neurological functions and its deficiency with dysfunction.”
In another recent study, researchers (Amato et al. 2010) found that both schizophrenia and Parkinson’s, along with others, were associated with “Latitude-Related Genes (LRGs).” They commented: “We found a strong enrichment of LRGs in the set of genes associated to schizophrenia.” They also concluded that, “several diseases show latitudinal clinals such as hypertension, cancer, dismetabolic conditions, schizophrenia, Parkinson’s disease and many more.”
As far as heart disease, various studies have also linked vitamin D exposure to heart disease. A study from researchers at Utah’s Intermountain Medical Center (Anderson et al. 2010) found, after reviewing 41,504 relevant patient records, that, ” The vitamin D levels were also highly associated with coronary artery disease, myocardial infarction, heart failure, and stroke…”
In addition, an extensive review by Dr. Colin Campbell (2006) found that countries with increased incidence of heart disease were also associated with an increase of animal-based diets among those countries.
In other words, A1-A2 research has not been corroborated by any official government study or review, nor is it substantiated by direct clinical research. The evidence given is circumstantial and based upon broad epidemiological research that associates populations with A1 milk that have many other associations common to them. There are many other possible associations to explain the diseases that A1 milk is purported to cause.
Furthermore, significant support and promotion of the A1-disease association appears to originate from and potentially profit a corporation whose patents control the conversion and delivery of A2 milk to the marketplace. While this association might be incidental, it does provide a dark cloud over the subject.
Amato R, Pinelli M, Monticelli A, Miele G, Cocozza S. Schizophrenia and Vitamin D Related Genes Could Have Been Subject to Latitude-driven Adaptation. BMC Evol Biol. 2010 Nov 11;10(1):351.
Annweiler C, Schott AM, Berrut G, Chauviré V, Le Gall D, Inzitari M, Beauchet O. Vitamin D and ageing: neurological issues. Neuropsychobiology. 2010 Aug;62(3):139-50.
McLachlan CN. beta-casein A1, ischaemic heart disease mortality, and other illnesses. Med Hypotheses. 2001 Feb;56(2):262-72.
Laugesen M, Elliott R. Ischaemic heart disease, Type 1 diabetes, and cow milk A1 beta-casein. N Z Med J. 2003 Jan 24;116(1168):U295.
Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth HE. Type I (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption. Diabetologia. 1999 Mar;42(3):292-6.
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Anderson JL, May HT, Horne BD, Bair TL, Hall NL, Carlquist JF, Lappé DL, Muhlestein JB; Intermountain Heart Collaborative (IHC) Study Group. Relation of vitamin D deficiency to cardiovascular risk factors, disease status, and incident events in a general healthcare population. Am J Cardiol. 2010 Oct 1;106(7):963-8.
Campbell TC, Campbell TM. The China Study: The Most Comprehensive Study of Nutrition Ever Conducted and the Startling Implications for Diet, Weight Loss and Long-term Health. Benbella Books, 2006.