Improving Health by Changing the Milk. A case study in how science works
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1 Improving Health by Changing the Milk. A case study in how science works Keith Woodford Professor of Farm Management and Agribusiness Lincoln University, New Zealand An address at Lincoln University to Biology Teachers 16 Nov 2009
2 A story of A1 and A2 milk The difference between A1 and A2 milk is a variant form of A1 beta casein. The A1 variant has been implicated in a range of diseases The question of whether or not we should be changing our milk from A1 to A2 lies at the intersection of science, health politics and industry politics. In NZ A2 milk is available in most cities if you seek it out; in Australia it is to be found in every Coles and Woolworths supermarket.
3 An overview The major medical conditions that have been associated with A1 beta casein are Type 1 diabetes, heart disease and symptoms of autism. Given the long latency periods of the implicated medical conditions (in particular Type 1 diabetes and heart disease) there are major challenges associated with double blind clinical trials. Accordingly, there is a need to focus on other scientific approaches, including epidemiology, biochemistry, pharmacology, immunology and animal trials.
4 Overview continued In bringing all of the evidence together, a key question arises: when does the cumulative evidence become sufficient to justify shifting away from A1 beta-casein? The A1/A2 issue also illustrates ethical issues associated with nondisclosure of information and selective use of evidence. According to LIC (the major supplier of dairy semen in NZ), shifting milk supplies to A2 (the original variant) can be done without compromising other breeding objectives. Should we therefore be doing it now?
5 A story on the move New evidence is rapidly emerging in relation to a range of other conditions. These include milk intolerance, eczema and mucus. And now there is powerful evidence coming out of Russia that has linked A1 beta casein to delayed development in babies
6 A1 beta -casein A1 beta-casein is only produced by some cows that are of European origin. The alternate casein is A2 beta-casein. African and Asian cattle are A2 unless they carry some European genes. Cattle can be either A1A1 or A2A2 or A1A2. Originally all cattle were A2. The incidence of the A1 allele varies by country and breed, even in Europe.
7 Milk and casein
8 The difference between A1 and A2 One amino acid in 209. The difference is a proline in A2 versus a histidine in A1 (at position 67). This affects the way the protein digests. A1 digestion releases, at least under some circumstances, a peptide (protein fragment) called betacasomorphin7 (BCM7). In comparison, A2 beta-casein either releases very little or no BCM7. BCM7 is a strong opioid with strong affinity for mu opioid receptors.
9 Release of beta-casomorphin-7
10 Milk, Casein and BCM7
11 Other species are A2-like in relation to their beta-casein structure Goats. Sheep. Yaks, camels, and reindeer. Humans! Nothing that I have said so far can be considered controversial. It is all in the peer reviewed scientific literature, and a link to where the sources are documented is provided at the end of this presentation.
12 Why has the mutant A1 gene survived in the bovine population? Founder effect? May not adversely affect cattle because of shorter lives or different digestive processes? BCM7 may lead to more passive calves? Other possibilities?
13 A little more on humans Human milk can produce small quantities of human BCM7. This is not the same as bovine BCM7 (10% the opioid strength and 10% the binding affinity of bovine BCM7). The role of human BCM7, either +ve or ve, is not clear. Possibly linked to post partum psychosis. An interesting literature is emerging. Focus here is on the much stronger bovine BCM7.
14 Where did it all start T1D in Samoan children in Samoa low versus Samoan children in NZ.(10X) A key dietary difference was milk. Casein was linked to diabetes in rats. But T1D very rare amongst Masai people in Kenya who drink lots of milk in traditional lifestyle. The key insightful question from Professor Bob Elliott: is there any difference in the casein of the milk that the Masai people were drinking compared to that drunk in NZ? The answer: Masai cattle are A2 whereas NZ milk is high in A1 beta-casein.
15 The Initial Work with NOD Mice Undertaken by Bob Elliott and colleagues. Funded by the NZ Dairy Board. Tested a range of diets including A1, A2, and a combination thereof. Diet Diabetes Rate A1 47% A2 0% A1A2 19% p<0.001 Limitations? - Blinding - Publication
16 Epidemiology: diabetes and A1 beta-casein KW1 (Laugesen and Elliott NZMJ 2003)
17 Slide 16 KW1 This is from wok undertaken by Dr Murray Laugesen and Bob Elliott and published in the NZMj in 2003 R2 =.84 Significant at p< Keith Woodford, 31/03/2008
18 Diabetes and milk protein. (Laugesen and Elliott, NZMJ, 2003)
19 Epidemiology: diabetes and A1 KW2 betacasein (Laugesen and Elliott NZMJ 2003)
20 Slide 18 KW2 This is from wok undertaken by Dr Murray Laugesen and Bob Elliott and published in the NZMj in 2003 R2 =.84 Significant at p< Keith Woodford, 31/03/2008
21 Heart disease and Type 1 diabetes McLachlan & Olsson, NZMJ 2003
22 Heart disease and A1 beta casein (McLachlan CNS, Medical Hypotheses 2001)
23 The importance of a leaky gut Health conditions linked to A1 beta-casein appear to have a common element: a leaky gut which allows peptides to pass through into the circulatory system. Leaky gut conditions include Coeliac disease, Crohn s disease, ulcerative colitis, stomach ulcers. All newly born babies have a leaky gut. The link to DPP4 (dipeptidyl peptidase 4).
24 Immunology Persons with T1D have enhanced levels of antibodies to beta-casein. This may simply be a manifestation of Type 1 diabetics being particularly sensitive to antibody formation. BUT: German research has shown that diabetics have higher antibody levels to A1 than A2 whereas controls have higher A2 than A1 (p<0.001). AND NZDRI (now Fonterra) and A2 Corporation joint patent reported people with T1D have IgG(1+3) antibodies that discriminate against A1 beta-casein vs. A2 beta-casein. (p=0.003)
25 Hypotheses but no proof. Diabetes Mechanisms BUT: we know that BCM7 is a strong opioid; at least in animals it crosses the blood brain barrier with ease and causes bizarre behaviour. BCM7 is also known to catalyse LDL oxidation. Therefore not surprising if there were antibodies to BCM7 and A1 beta-casein. There is a homologous (similar) amino acid sequence in the GLUT2 glucose transporting molecule inside the insulin producing cells. The logic is that the insulin producing cells within the pancreas are therefore being attacked by misdirected friendly fire. Consistent with current scientific knowledge.
26 Human studies No human clinical trials specifically comparing the diabetogenic effects of A1 and A2 beta-casein. In Finland genetically predisposed people drinking more than 540ml of milk per day >5 X as likely to become diabetic as those drinking less. (p<0.01) (cohort study) Preliminary data from TRIGR trial that babies aged 6-8m fed casein hydrolysate cf standard infant formula less likely to develop positivity for islet cell antibodies (p=0.02) and at least one auto-antibody (p=0.03).
27 More on animals The Food and Diabetes trial (FAD) Multi country using NOD mice in NZ and Britain, BB rats in Canada. Diets supplied by NZDRI Results published in Diabetologia Published paper claims that the results did not support Bob Elliott s earlier work with NOD mice.
28 More on the FAD trial Known >1 yr before paper submitted for publication that half of the A2 diets seriously contaminated by BCM7. It was known to at least four of the nine authors including the author from NZDRI (Fonterra) who supplied the diet. There has never been any public knowledge of this contamination. Once the contaminated diets are removed from the analysis then the results do broadly support Bob Elliott s earlier work.
29 The FAD scandal Some of FAD authors have used this paper to widely proclaim against A1 A2 hypothesis in a range of forums. Most widely used counter evidence within the dairy world internationally. A scandal which Diabetologia needs to take up but they have declined my request to do so. The documentary evidence is irrefutable. It really is a scientific scandal.
30 Bringing the diabetes story together The strength of the diabetes story is the cumulative evidence across the scientific disciplines. Epidemiology Animal trials Biochemistry Pharmacology Immunology Human studies Mechanisms When is enough enough
31 More on heart disease Rabbits fed A1 developed arterial plaque on the aorta whereas those fed A2 did not. (P<0.01) High milk (Sippy type) diets for peptic ulcers led to 2.5 X deaths from heart attacks cf ordinary diets in UK and 6 X in USA. For each of these p<.01. BCM7 oxidises LDL. (and oxidised LDL is a recognised risk factor) Babies fed formula have up to 10 X antibodies to oxidised LDL cf those breastfed.
32 Autism and schizophrenia BCM7 injected into rats passes freely through blood/brain barrier. BCM7 injected in rats causes bizarre behaviour akin to autistic symptoms. BCM7 is found in the urine of many autistic people. This BCM7 can only come from milk. Symptom improvement when milk removed from diet. Linked to leaky gut.
33 The counter attack Papers to International Dairy Federation by Fonterra scientists arguing against A2. But never published in peer reviewed literature. Media releases Below the radar communications Industry associations not always disclosed General lobbying including government: we must not damage the dairy industry.
34 Milk intolerance Observational evidence: nausea, bloating, diarrhoea, some allergies Goat milk Cheese Mucus and mucins
35 NZFSA and the Swinburn Review In 2003 the NZFSA commissioned a review of A1/A2 by Professor Swinburn with the report published in August The focus was on epidemiology and human trials and not on the underlying science. Despite these limitations the essential message was one of uncertainty. There was strong evidence but there was no proof. Swinburn purposefully did not say anywhere that milk was safe. However the NZFSA claimed that his report showed there was no safety issue with either milk.
36 A quote from Professor Swinburn in a letter to NZFSA, August 2004 if I had a child with Type 1 diabetes and was due to have another and I could easily obtain and afford A2 milk or formula, I would certainly use it for the next child because the cost/benefit is low because of the potentially very large benefit of preventing Type 1 diabetes.
37 The cost of change LIC could, within 48 hours, respond to a market directive to move to A2 milk (i.e. only put A2 bulls forward for collection ). This would mean that within eight to ten years, virtually every cow in New Zealand would be A2. This shift - if directed by consumer demand could be done without compromising other genetic qualities (LIC, Your Choice, Spring 2007, p23) NZ is already drifting to A2 at a significant rate but this is through serendipity. Very unlikely to be happening elsewhere.
38 Swinburn s 2008 message (14 April) The time to change the dairy herd to A2 is right now
39 The Slorach Report (29 April 2008) Found that release of Swinburn report lacked transparency, and some of the decisions around the release, such as releasing it on precisely the day that Swinburn had told them he would be unavailable to take media calls, were difficult to justify. Reported that NZFSA were now saying that their all milk is safe claim related to conventional food safety claims (i.e. sickness and hospitalisation after eating a product) and not to health conditions.
40 European Food Safety Report Found in Jan 2009 that there was no proof of a cause and effect. In narrow terms this finding was defensible if the criterion is the gold standard of double blind clinical trials on humans If we demanded that standard elsewhere we would still be saying there is no proof that smoking is dangerous
41 The difficulty of processing new information The history of science tells us that all significant scientific break throughs are fought against. Very easy to process information supporting an existing stance differently than for information that challenges that stance
42 The latest information Kost NV et al (2009). At press. doi:10:1016/j.peptides (At press in the journal Peptides and currently available online) Have developed a technique for measuring BCM7 in the blood. (This is a first.) Have found nearly all children fed formula have high BCM7 in the blood. Approx 30% of children on formula suffer developmental delay. This developmental delay correlates very closely with ability to eliminate BCM7 from the blood within a few hours after feeding.
43 For further information For online purchase go to: Or get the book from the library (there are lots of library copies)
44 For a written copy of my paper to the International Diabetes Federation (2 April 2008) go to:
45 For a copy of this powerpoint me at: keith.woodford@lincoln.ac.nz
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