This article was to be published in The Conversation but was
pulled at the last minute as senior editors "felt that the
interests of associated commercial parties, who might benefit from
dissemination of the article, were too great". It has since been
published in several other publications.
Authors: Keith Woodford,
Agricultural Management Group, Lincoln University, Christchurch,
New Zealand, & Boyd Swinburn,
School of Population Health, University of Auckland, Auckland, New
Type 1 diabetes, an autoimmune disease in which the body attacks
its own insulin-producing cells, is on the rise globally.
Early evidence of an association between type 1 diabetes and a
protein in cow milk, known as A1 beta-casein,
was published in 2003. However, the notion that the
statistically strong association could be causal has remained
As part of a seven-person team,
we have reviewed the overall evidence that links A1 beta-casein to
type 1 diabetes. Our research brings forward new ways of
looking at that evidence.
Different types of diabetes
Type 1 diabetes is the form of diabetes that often manifests
during childhood. The key change is an inability of the pancreas to
produce insulin, which is essential for transporting glucose across
internal cell membranes.
There is common confusion between type 1 and the much more
common type 2 diabetes. Type 1 diabetes is an autoimmune disease.
This means that the immune system attacks the body's own cells.
Insulin-producing cells in the pancreas are then destroyed by
There is no accepted lifestyle change that will prevent or cure
type 1 diabetes and daily insulin injections are required
In contrast, people who develop type 2 diabetes still produce
some insulin, but the liver and muscles become resistant to
insulin's ability to move glucose out of the blood and into the
Type 2 diabetes is primarily a disease of middle-aged and older
people and is related to excess weight, diet and lack of physical
A1 beta-casein comes from European-type
If A1 beta-casein is indeed triggering type 1 diabetes, then
this would be of profound importance. Globally, there are
new cases diagnosed in young people every year, with many
additional cases diagnosed in adults.
Cows of European origin are the only source of A1 beta-casein.
It is the result of a mutation, probably some thousands of years
ago. Some of these cows produce beta-casein that is all A1, others
produce a mix of A1 and another type known as A2, and others
produce only the A2 type.
Goats, sheep, Asian cattle, buffalo, camels and indeed humans
produce milk only of the A2 type.
A1 beta-casein, on digestion, releases a peptide (protein
fragment) which has opioid and inflammatory characteristics. The
protein fragment is called beta-casomorphin-7 ("caso" from casein,
"morphin" from morphine-like, and 7 to indicate the fragment
contains seven amino acids).
The release of this protein fragment is accepted science; it is the
implications that have been controversial. There is scientific
literature that links A1 beta-casein to multiple health conditions,
but here, we restrict ourselves to type 1 diabetes.
Evidence but no definitive proof
The evidence in our paper comes from 71 studies covering
population epidemiology, animal trials, in vitro laboratory
experiments, biochemistry and pharmacology.
Our assessment is that the evidence is highly suggestive that A1
beta-casein is associated with the onset of type 1 diabetes, but
proof remains elusive.
There have been no clinical trials specifically investigating a
long-term diet free of A1 beta-casein.
Such trials would be very expensive and difficult, but not
impossible, to conduct.
People who are genetically susceptible to developing type 1
diabetes would need to be identified at birth and half of them
randomly allocated to a diet free of A1 beta-casein for many
Clinical trials are very powerful when the effects are quickly
However, they are seldom practical when outcomes are caused by
prolonged exposure to a particular food or other environmental
factor, and where effects may take many years to manifest.
In these situations, other methods based on epidemiology,
often combined with insights about biological mechanisms, provide
the underpinnings for public health actions.
Type 1 diabetes varies between countries
Studies across countries show very high correlations between type
1 diabetes incidence (with a variation of 280-fold) and intake of
A1 beta-casein (more than five-fold variation).
Figure 1: Correlation between A1 β-casein supply per capita
in 1990 and type 1 diabetes incidence (1990-1994) in children aged
0-14 years in 19 countries. Original source
Such country-level studies are sometimes criticised because
statistical associations between populations do not necessarily
apply at the individual level.
However, the A1 beta-casein results are very stable in that they
are not dependent on one or two outlier countries and no-one has
come up with an alternative explanation as to what could explain
such very high correlations.
In our paper, we report recent evidence from China where type 1
diabetes was almost unknown in the past. Now, it is increasing
rapidly along the developed eastern seaboard. There is published
data for two cities.
In Shanghai, the incidence (new cases) increased at
14.2% compound rate each year between 1997 and 2011.
In Zhejiang (a major city south of Shanghai) it
increased at 12% percent compound rate per annum
between 2007 and 2013. These increases are mirrored by China's
increased per capita dairy consumption from 6kg in 1992 to 18kg in
2006, and with further substantial increases thereafter.
There are no other apparent explanations for this rapid rise in
Type 1 diabetes in China.
Bovine milk has previously been identified as a potential risk
factor for Type 1 diabetes.
There have been multiple trials comparing breast milk to
formula, and also comparing alternative ages of first introduction
to bovine milk. But clear answers have been elusive.
Those inconsistent results are not surprising if the problem is
indeed A1 beta-casein, which has such variability of levels between
None of these trials have specifically compared A1 beta-casein
to A2 beta-casein, and none of the trial treatments have been long
term post-weaning. In essence, these trials have lacked the
While A1 beta-casein may be the primary causal agent, there are
probably many predisposing factors.
A genetic predisposition has been known for some time but other
factors such as
infections and antibiotics which affect the intestinal
mucosal barrier may prime the immune system to turn against the
Vitamin D levels may also be predisposing in some
situations, although the evidence for this is limited.
Figure 2: Proposed Type 1 diabetes mechanisms (Source:
It is clear that none of the multiple predisposing factors are
capable of being causal by themselves; instead they create the
environment where a trigger can do its damage.
Accordingly, the key is to remove either the trigger or all the
predisposing factors. When predisposing factors are multiple, it is
usually easiest to remove the key trigger.
Public health and personal choice
It is feasible to breed all dairy herds to produce milk free of
A1 beta-casein. The catch is that it would take at least ten years
in most countries, even if all dairy farmers used only A2 bulls and
A2 semen in breeding programmes from now on.
However, cow milk free of A1 beta-casein is increasingly
available in many Western countries, including New Zealand,
Australia, the USA and Britain. Goat and sheep milks are other
options for those seeking milk that is free of A1 beta-casein.
In the absence of definitive proof, consumers have to make their
own choices. This is particularly important in situations where
there is a family history of type 1 diabetes.
However, the increasing incidence means that type 1 diabetes is
increasingly showing up in families without that prior family
history, and this is particularly relevant to parents of infants
and young children.
An open access version of the research is available
from the study
The evidence for milk and, particularly A1 β-casein,
as a primary dietary trigger for type 1 diabetes is intriguing
although causation remains unproven. The ecological evidence across
populations is particularly strong. Exclusive breastfeeding is
widely regarded as being protective against type 1 diabetes in
early infancy, but its benefits may be lost if the mother
supplements breast milk with cows' milk formula, or if the duration
of breastfeeding is too short. It is also conceivable that some
dietary triggers might cross into breast milk. These factors might
contribute to the inconsistencies in the reported associations
between breastfeeding and type 1 diabetes. Latitude acting as a
proxy for vitamin D exposure has been suggested as a potential
causal factor, but hypotheses linking vitamin D as a causative
trigger in type 1 diabetes have been unrewarding. Thus, we suggest
that factors such as vitamin D may act as influencing or modifying
factors, but not causal factors. Furthermore, the geographical
variability and the chronological changes in type 1 diabetes
incidence suggest that changes to influencing factors and
permissive gut factors may have altered (for example, gut
microbiome profiles), contributing to the increasing incidence of
type 1 diabetes.
If A1 β-casein is indeed the dominant causal trigger, then the
apparent inconsistent and therefore puzzling results with previous
milk studies may be explained. For example, the widespread
geographical variation in A1 to A2 β-casein ratio of milk products
combined with variable β-casein content of infant formulas, a
consequence of different casein to whey ratios of the formulations,
may complicate the interpretation of the data.
There are particular challenges associated with
prospective studies investigating milk per se as
causative of type 1 diabetes. These challenges relate to the
ubiquity of milk in the diets in developed countries and the
long-term nature of any trials. Influencing factors include the
potential protective effects of breastfeeding and its duration, and
whether or not all bovine milk is excluded from the diet of the
mother as well as the baby. However, the potential role of A1
β-casein as a causative trigger for type 1 diabetes could be
resolved by prospective studies in genetically at-risk individuals,
using milk diets from birth that do not contain A1 β-casein, but
which contain β-casein of the A2 type exclusively.