out the beta-casein evidence
August, 2014 byFairfax NZ Sunday Star Times
Professor Keith Woodford: I advocated that the mainstream dairy
industry should convert New Zealand herds away from the production of A1
beta-casein. To not do so creates unnecessary long term risk to the
industry. However, the mainstream industry remains locked into a
In this article I
will therefore briefly review some of the major strands of health
evidence. I cannot cover it all – it took me a whole book to do so
back in 2007. Since then, there has been a lot more evidence forthcoming.
In assessing the evidence, it is helpful to
recognise that A1 beta-casein is the consequence of a historical
mutation. Goats, sheep camels, buffalo, Asian cattle and humans produce
beta-casein that is totally of the A2 type. It is only cows of European
ancestry which produce A1 beta-casein.
In modern dairy herds, the proportion of A1
beta-casein varies by country, by breed and by herd. In New Zealand,
there has been a slow drift towards A2. About 40 percent of New Zealand
cows now produce beta-casein that is all A2, and most of the rest produce
a 1:1 ratio of A1 and A2 beta-casein. A few animals produce only A1
None of this would matter if it were not that A1
beta-casein on digestion releases a peptide (a protein fragment) called
beta -casomorphin-7 (BCM7), whereas this does not occur with A2
beta-casein. Even the European Food Safety Report in 2009 conceded that
this is correct. There is also no doubt that this peptide has opioid
characteristics. It is a well-established scientific fact.
However, what has remained controversial until
recently has been whether or not the BCM7 can pass through into the
blood. Russian researchers have now shown quite clearly that it does pass
into the blood of babies fed infant formula. They have also shown that a proportion
of these babies are unable to metabolise the BCM7 efficiently between
feeds and these particular babies have delayed psycho-motor
Russian workers have also found BCM7 in the urine
of all children on normal milk diets. Polish researchers have even found
that mothers who are themselves drinking cow milk can pass bovine BCM7 to
their babies in breast milk.
The original evidence implicating A1 beta-casein came
from Professor Bob Elliott from Auckland University.
He noted that Samoan children brought up in Samoa had
a minimal level of Type 1 diabetes whereas children of
Samoan ethnicity in New Zealand are vulnerable. He looked
for differences in lifestyle, and identified exposure
to cow milk as a possibility. Subsequently working with
Dr Murray Laugesen, he showed that across the developed
world more than 80% of the between-country variations
in Type 1 diabetes could be explained by per capita intake
of A1 beta-casein. Corran McLachlan showed similar correlations
between intake of A1 beta-casein and heart disease. The
correlations are statistically very strong and no alternative
explanation for these between-country differences has
stood the test of time.
A human clinical trial from Curtin University in
Australia, recently published in the European Journal of Clinical
Nutrition, found that there were statistically significant differences in
digestive symptoms between milks containing A1 and A2 beta-casein. This
has drawn attention back to some of the animal trials for explanations.
For example, a New Zealand trial with rats, undertaken by AgResearch and
co-funded by the New Zealand Government and The a2 Milk Company, and
published earlier this year, found increased levels of an inflammation
marker MPO in the colon on the A1 diet. I am a co-author on both the
Curtin and AgResearch papers.
A similar study with mice, published last year in
the European Journal of Nutrition, found comparable inflammation results.
That study also found strong immunological responses to the A1, with
greatly increased levels of antibody production.
The New Zealand ‘AgRats’ study also
found, as expected, that the opioid effects of BCM7 from A1 beta-casein
slowed down the passage of food through the rat intestines. Intriguingly,
the A1 beta-casein also significantly increased the release of an enzyme
called DPP4. The reason this is so intriguing is that the modern gliptin
drugs, now widely used to control Type 2 diabetes, act by inhibiting this
enzyme, whereas with A1 beta-casein the level increased.
There is a lot more research of relevance,
including arterial plaque in rabbits and increased antibodies to oxidised
LDL in humans. I now have several hundred published studies of relevance
in my database. There is also a stream of additional studies in the pipeline
about which I am very excited. There is no chance this issue will go
Next week, in the last of this series on A1
beta-casein, I will explain how to eliminate production of A1 beta-casein
through breeding. I will also look again at the industry politics of A1
beta-casein and why the industry is so defensive.
BCM7 in the milk we drink
Woodford, professor of farm management at Lincoln
University, has reviewed a
hundred scientific papers on the peptide betacasomorphin BCM7 in A1 milk,
raising concerns about possible health effects. Research in 2003 by
Laugesen and Elliott (see below) is featured, but recommendations by
Professors Beaglehole, Jackson and Swinburn in 2003 for more research
have yet to be implemented. The issue is not about whether people should
drink milk but about whether people should be able to buy A1-free milk.
A2 milk sales have increased in the North Island,
but South Islanders cannot yet buy A2 milk at a reasonable price.
Devil in the Milk Illness, health and politics
A1 and A2 milk. Professor Keith
Woodford, Craig Potton Publishing
ISBN 978-1-877333-70-5 – Oct. 07)
Data on BCM7
in New Zealand dairy products
Neither Fonterra nor A2 Corporation has published
data on the BCM7 content of their milk products. The NZ Food Safety
Authority repeats that milk is safe, but offers no test results to show
that infant formula, for example, is free of BCM7.
Woodford’s book offers more than enough
evidence to apply the precautionary principle, and he urges dairy
farmers, at no extra cost, to use pure A2 semen from now on. For whatever
one’s position on the science, once dairy farmers decide to
inseminate their cows with pure A2 semen rather than with A1, the A1
content of New Zealand milk will decline to near zero (Guernsey Island
levels) within 10 years. If Fonterra offered a slight premium at the farm
gate for A2 milk, this goal would be reached much sooner.
– is it safe?
The NZ Food Safety Authority’s
re-iteration that milk is safe, is a generalization. Great care is taken
to pasteurize it and keep it safe from communicable disease. With respect
to non-communicable disease, milk, like most food additives and flavours,
is Generally Regarded As Safe (GRAS). It is not, however, completely
safe. For example, milk including A2 milk, can cause serious milk
1. Smith WB,
Thompson D, Kummerow M et al. Letter to MJA 2004 181 (10) 574.)
Research to reduce heart disease and diabetes
Laugesen and Elliott’s 2003 research
paper confirms a high degree of correlation between A1 beta casein and
heart disease and diabetes, at population level. This has raised the
possibility that the type of casein in the fresh milk supply could be a
risk factor. But proof of this
concept is elusive. As Beaglehole and Jackson said in the accompanying
NZMJ editorial, further research is recommended.
A1 but not A2 milk breaks down to form the peptide
casomorphin-7. Much more needs to be known as to the final fate in the
body of this peptide, known to be bioactive.
research paper: www.nzma.org.nz/journal/116-1168/
NZ MJ editorial www.nzma.org.nz/journal/116-1168/
Fonterra’s comment: www.nzma.org.nz/journal/116-1169/
The authors’ reply: www.nzma.org.nz/journal/116-1170/
disease and diabetes type 1 are commoner in North Europe, and one possible explanation may lie in the
genetics of the cow and type of milk consumed. A1 milk differs very
slightly from A2 milk in the composition of one of its main proteins,
beta casein. A1 is a genetic
variant of A2 milk.
A1 milk was
commoner from black and white (Holstein-Friesian herds) or red and
white herds, as found in Northern Europe, and A2 more in brown herds as
in Southern Europe and the Channel
Island breeds. These associations with skin colour have become
blurred in recent decades by widespread artificial insemination from Holstein bulls. The proportion of A1 milk in the town
supply still varies considerably across countries and somewhat over the
Further thoughts on A1 and A2 milk
Laugesen and Elliott found that
while differences in A1 milk consumption can explain differences in
heart disease and diabetes type 1 between countries, they do not
explain why diabetes type 1 is increasing in almost all countries.
Casomorphin 7 in A1 milk if glycated can be absorbed orally and have
adverse immune effects. Recent data
support the hypothesis that non-enzymatic pathways (glycation and
oxidation) are involved in the pathogenesis of tissue damage in
Infant formula is high in advanced glycation end products
(AGEs), which can cause diabetes in mice. A diet low in AGEs is
protective in mice.
RB. Diabetes – a man-made disease. Med Hypotheses.
2006;67(2):388-91. Epub 2006 Mar 10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16530335&query_hl=1&itool=pubmed_docsum
Health New Zealand Ltd is interested
in sponsors for further research on this topic.
A1 and A2 milk – what
is the difference?
New Zealand on its own initiative, carried out research on the relation
of A1 milk to heart disease, and type 1 diabetes, to prove or disprove
the existence of correlations noted by Professor Bob Elliott and the
late Dr Corran McLaughlin, later founder of A2 Corporation www.A2corporation.com which promotes A2 milk. If this
correlation was true, it had importance for investors, for New Zealand, for public health and disease
prevention. If not, then the
sooner it was disproved the better. Fonterra’s Research Institute
put its library at our disposal. Preliminary work showed the presence
of strong correlations. The work
was then completed with the assistance of A2 Corporation. The
country-level correlations are not proof of concept, for which
individual-level data were needed. This we acknowledge in our paper.
of the Laugesen and Elliott paper in January 2003 resulted in several
papers by Fonterra staff (Hill, Crawford) and nutritionists Mann
(Otago) and Trusswell (Sydney), all critical of the A1/A2 concept.
Cardiovascular epidemiologists, Beaglehole and Jackson, who wrote the
editorial accompanying the paper, and cardiovascular nutritionist
Swinburn who reviewed research to date on the issue, took the view that
although correlations have their pitfalls, this correlation was of
potentially great importance and deserving of further
(commercially-funded) research to prove or disprove it.
the paper below was published in 2003, A2 milk was not available in New Zealand, and even today it is only available in
certain supermarkets. To a limited extent then, this research has
secured greater consumer choice. As most of the top bulls are now pure
A2, (whether by accident or design), the A2 content of the town milk
supply will gradually increase.
Med J 24 January 2003;
vol 116, no. 1168. Full text at www.nzma.org.nz/journal
Ischaemic heart disease, Type 1 diabetes, and cow milk A1
Murray Laugesen and Robert Elliott
To test the correlation of per capita A1
β-casein (A1/capita) and milk protein with: 1) ischaemic heart
disease (IHD) mortality; 2) Type 1 (insulin-dependent) diabetes
mellitus (DM-1) incidence.
A1/capita was estimated as the product
of per capita cow milk and cream supply and its A1 β-casein
content (A1/ β) (calculated from herd tests and breed
distribution, or from tests of commercial milk), then tested for
correlation with: 1) IHD five years later in 1980, 1985, 1990 and 1995,
in 20 countries which spent at least US $1000 (purchasing power
parities) per capita in 1995 on healthcare; 2) DM-1 at age 0–14
years in 1990–4 (51 were surveyed by WHO DiaMond Project; 19 had
A1 data). For comparison, we also correlated 77 food, and 110 nutritive
supply FAO (Food and Agriculture Organization)-based measures, against
IHD and DM-1.
For IHD, cow milk proteins (A1/capita, r
= 0.76 , p <0.001; A1/capita including cheese, r = 0.66; milk
protein r = 0.60, p = 0.005) had stronger positive correlations with
IHD five years later, than fat supply variables, such as the
atherogenic index (r = 0.50), and myristic, the 14-carbon saturated fat
(r = 0.48, p <0.05). The Hegsted scores for estimating serum cholesterol
(r = 0.42); saturated fat (r = 0.37); and total dairy fat (r = 0.31)
were not significant for IHD in 1995. Across the 20 countries, a 1%
change in A1/capita in 1990 was associated with a 0.57% change in IHD
A1/capita correlations were stronger for
male than female mortality. On multiple regression of A1/capita and
other food supply variables in 1990, only A1/capita was significantly
correlated with IHD in 1995.
DM-1 was correlated with supply of:
A1/capita in milk and cream (r = 0.92, p <0.00001); milk and cream
protein excluding cheese (r = 0.68, p <0.0001); and with A1/β
in milk and cream (r = 0.47, p <0.05). Correlations were not
significant for A2, B or C variants of milk β-casein. DM-1
incidence at 0–4, 5–9 and 10–14 years was equally
correlated (r = 0.80, 0.81, 0.81 respectively) with milk protein
supply. A 1% change in A1/capita was associated with a 1.3% change in
DM-1 in the same direction.
Cow A1 β-casein per capita supply
in milk and cream (A1/capita) was significantly and positively
correlated with IHD in 20 affluent countries five years later over a
20-year period – providing an alternative hypothesis to explain
the high IHD mortality rates in northern compared to southern Europe.
For DM-1, this study confirms
Elliott’s 1999 correlation on 10 countries for A1/capita,1
but not for B β-casein/capita. Surveys of A1 β-casein
consumption in two- year-old Nordic children, and some casein animal
feeding experiments, confirm the A1/capita and milk protein/capita
correlations. They raise the possibility that intensive dairy cattle
breeding may have emphasised a genetic variant in milk with adverse
effects in humans. Further animal research and clinical trials would be
needed to compare disease risks of A1-free versus ‘ordinary’