may set off diabetes for genetically vulnerable.
protein A1 beta-casein that's found in cows' milk could
trigger type 1 diabetes in people with genetic risk factors,
a new report warns.
report refers to the 2003 Laugesen and Elliott study shown
below, and is based on 71 papers.
who are genetically susceptible would need to be identified
and half of them randomly allocated to a diet free of
A1 beta casein for many years, according to Swinburn and
JSJ, Woodford, Elliott, Swinburn, Dwyer et al.
and Diabetes 2017: 7: e274. Corresponding author Karen.Dwyer@deakin.edu.au
Teasing 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 defensive position.
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
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 beta-casein.
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
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
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 away.
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
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
Devil in the Milk Illness, health and politics
A1 and A2 milk.
Professor Keith Woodford,
Craig Potton Publishing ISBN 978-1-877333-70-5 –
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 allergy.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
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.
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.
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 years.
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 diabetes mellitus.
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.
Elliott 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
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
the A2 Milk Company 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’