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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.
Milk
– 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
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.
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Health New
Zealand’s
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/
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Heart
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
years.
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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.
See 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
Health New Zealand Ltd is interested
in sponsors for further research on this topic.
A1 and A2 milk – what
is the difference?
Health
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.
Publication
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.
When
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.
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J NZ
Med J 24 January 2003;
vol 116, no. 1168. Full text at www.nzma.org.nz/journal under
Archived
Ischaemic heart disease, Type 1 diabetes, and cow milk A1
β-casein

Murray Laugesen and Robert Elliott
Abstract
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Aim
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.
Methods
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.
Results
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 in 1995.
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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.
Conclusions
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’ milk.
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