We would like to respond to Jeremy Hill’s letter published in the previous issue of the Journal (http://www.nzma.org.nz/journal/116-1169/346/).

As Hill notes, we found that A1 β-casein correlated significantly with IHD mortality.1 This, we now find, also applies to non-fatal IHD, at least in males. For 13 WHO MONICA (Monitoring trends and determinants in cardiovascular disease) study countries (all healthcare affluent, and including New Zealand), we had sufficient data to test for correlation.2 A1 β-casein per capita in the 1985 food supply correlated significantly with the non-fatal, fatal, and total IHD events rates for 35 to 64-year-old males 4–9 years later. This was not true for females, nor for serum cholesterol, smoking, or body mass index in males.

Tobacco consumption was not correlated with IHD mortality at population level – heavy smokers’ risk is only 20% higher, and so most smoker IHD deaths occur among moderate or light smokers.3 As the consumption per smoker varied greatly between countries,4 reduction in consumption may not reap a proportionate reduction in IHD mortality.

In children, besides consumption of cow milk, likely factors include genetic predisposition, impaired gut immunity, and enterovirus infection.5 Higher levels of β-casein antibodies have been found in DM-1,6 specifically against A1 β-casein.7 The quantity of cow milk consumed during childhood has been associated with DM-1;8 and infants in a high risk group for DM-1 and exposed to cow milk formula had increased auto-antibodies against bovine and human insulin.9

Inclusion of cheese per capita (mostly eaten by adults) did weaken the association between milk per capita and childhood DM-1 in our study. Child cheese consumption may vary more from adult cheese consumption internationally than child milk consumption varies from adult milk consumption. Also, choice of cow breeds, manufacturing processes, and market share of different brands, long storage before sale, and wastage, may affect national A1 β-casein per capita in cheeses differently from milk.

As we stated, the temporal decline in per capita (mainly adult) milk supply cannot explain the rise in child DM-1 incidence, but what might explain the rise are the trends in child A1 β-casein consumption in response to the greater range of pre-cooked foods and yoghurts now available.

Hill refers to an animal feeding trial in diabetes-prone rodents,10 a trial designed to determine whether DM-1 incidence differed between diets supplemented with A1 and A2 β-casein respectively. In the (BB) rats there was a difference, but not in the (NOD) mice. The latter finding was at variance with earlier findings.11 That rodent chow containing no milk protein had the highest DM-1 incidence in both species is interesting, but young humans consume milk not chow. Further animal research alone will never be sufficient to provide the basis for public policy.12

A1, B and C variants of β-casein are similar in that all have histidine at position 67 of the molecule, instead of the proline present in the A2 variant. In the case of A1, this is the sole difference, whereas there are further differences in the B and C variants. This may be why A1 but not B and C variants are correlated with DM-1. The B and C variants are in any event usually very minor components, and estimates of their prevalence are not available for some countries. Elliott was author of both of the studies that show this ‘+B and +C’ difference. Our study includes more countries, all surveyed during the same six-year period.

We need more and better data in the public domain, aided perhaps by the International Dairy Federation or Fonterra itself, monitoring and publishing A1 β-casein content in milk and other foods, by brand, country, and year.

The correlations we have described are far from conclusive, but cannot be ignored. They merit further research on the milk-drinking habits of those with and without IHD; and similarly for DM-1.