Download G-2025 Milk, Why American Milk Is Different

Milk: Why American Milk Is Different
Note: A1 protein also is known as A1 beta-casein, and A2 protein also is known as A2 betacasein.
It recently was speculated that A1 protein, most often found in milk produced by Holstein cows,
is to blame for symptoms of “lactose intolerance.” A1 is not as prevalent in milk from Jersey,
Guernsey, and most Asian and African cows; in these cows’ milk, the A2 protein is in highest
concentrations. Goat milk and human milk contain only A2 protein, while modern cows are
purely A2, purely A1, or a mix of A1 and A2.
An Aukland-based company, A2 Corp, has sold A2 milk in New Zealand and Australia for the
past 10 years, and it now accounts for 8% of Australia’s dairy market. In 2012, A2 Corp
introduced its milk in the United Kingdom, where it sells for about 20% more than conventional
milk. A2 Corp recently has announced it will expand into the American market in the near
future.
A review completed by the European Food Safety Authority in 2009 found no link between A1
milk and gastrointestinal symptoms. The Australia Queensland Health Dept fined the marketers
of A2 milk $15,000 in 2004 for making false and misleading claims regarding the health benefits
of A2 milk.
Some people have pointed the finger at A1 for increasing the risk of a large number of health
conditions, including heart disease, diabetes, and autism. A1 protein releases an opioid (BCM7)
when digested. This excerpt from a letter published in the September-October 2012 issue of the
Indian Journal of Endocrinology and Metabolism succinctly summarizes the concerns:
“BCM7 is suggested to be associated as a risk factor for human health hazards as
it can potentially affect numerous opioid receptors in the nervous, endocrine and
immune system. It is also known to be an oxidant of low dietary lipoproteins
(LDL) and oxidation of LDL is believed to be important in formation of arterial
plaque. Epidemiological evidences claim that consumption of beta-casein A1 milk
is associated as a risk factor for type-1 diabetes, coronary heart disease,
arteriosclerosis, sudden infant death syndrome, autism, schizophrenia etc.1,2 A
broad range of studies from American and European investigations has shown
reduction in autistic and schizophrenic symptoms with decrease in A1 milk
intake.3 Further, animal trials have also supported the linking of type-1 diabetes
to milk exposure in general and A1 beta-casein in particular.
“Populations, which consume milk containing high levels of β-casein A2 variant,
have a lower incidence of cardiovascular disease and type-1 diabetes. The A1/A2
hypothesis is both intriguing and potentially very important for public health if it
is proved correct. It should be taken seriously and deeper research is needed to
verify the range and nature of BCM7 interactions with the human gastrointestinal
tract and whole organism. This requires more of animal trials and generation of
data on human subjects having the problems related to A1/A2 beta-casein milk
consumption.”
1. Laugesen M, Elliott R. Ischaemic heart disease, type 1 diabetes, and cow milk A1 beta-casein.
N Z Med J. 2003;116(1168):U295.
2. Tailford KA, Berry CL, Thomas AC, Campbell JH. A casein variant in cow’s milk is
atherogenic. Atherosclerosis. 2003;170(1):13-19.
3. Cade R, Privette M, Fregly M, et al. Autism and schizophrenia: intestinal disorders. Nutr
Neurosci. 2000;3:57-72.
In 1993, Bob Elliott, a professor of child health research at the university of Aukland, verbalized
his belief that A1 milk is possibly to blame for the high incidence of type-1 diabetes among
Samoan children growing up in New Zealand. Later, he and a colleague found a strong
correlation between consumption of A1 milk and the prevalence of diabetes and heart disease in
20 countries. However, critics say that diet, lifestyle, and exposure to vitamin D from sunlight
might explain the relationship, rather than the milk consumption.
Elliott also published a study in 1997 showing that A1 protein caused mice to develop diabetes.
A peer-reviewed study carried out at the National Dairy Research Institute in India in 2012 found
that mice fed A1 beta-casein overproduced enzymes and immune regulators that were found to
link to heart disease and autoimmune diseases in other studies.
Recently, research done at Northwestern University found that the presence of BCM7 in gut cells
creates a shortage of antioxidants in neural cells in cell culture; this condition was linked to
autism by other research. This study was underwritten in part by the A2 Corp. A 2009 study
showed that formula-fed (formula containing A1 protein) infants were slower to develop muscle
tone and psychomotor skills compared to infants who were fed only breast milk (breast milk
contains A2 protein). A 2011 study implicated BCM7 in sudden infant death syndrome. A2 Corp
also sells an A2-only infant formula in Australia, New Zealand, and China.
A critique of the A1/A2 hypothesis published in the European Journal of Clinical Nutrition in
2005 pointed out that:
“For both DM-I [diabetes mellitus type 1] and CHD [coronary heart disease],
the between-country correlation method is shown to be unreliable and negated by
recalculation with more countries and by prospective studies in individuals. The
animal experiments with diabetes-prone rodents that supported the hypothesis
about diabetes were not confirmed by larger, better standardised multicentre
experiments. The single animal experiment supporting an A1 beta-casein and
CHD link was small, short, in an unsuitable animal model and had other design
weaknesses.”
References and recommended readings
Harkinson J. You’re drinking the wrong kind of milk. Mother Jones Web site.
http://www.motherjones.com/environment/2014/03/a1-milk-a2-milk-america. Published March
12, 2014. Accessed April 23, 2014.
Sodhi M, Mukesh M, Kataria RS, Mishra BP, Joshii BK. Milk proteins and human health:
A1/A2 milk hypothesis. Indian J Endocrinol Metab. 2012;16(5):856. doi:10.4103/22308210.100685.
Truswell AS. The A2 milk case: a critical review. Eur J Clin Nutr. 2005;59(5):6213-6231.
http://www.nature.com/ejcn/journal/v59/n5/abs/1602104a.html. Accessed April 23, 2014.
Contributed by Elaine Koontz, RDN, LD/N
Review Date 4/14
G-2025