Noch mal was zum Thema Beta-Casein A1:

N Z Med J. 2003 Jan 24;116(1168):U295.

Comment in:
N Z Med J. 2003 Feb 21;116(1169):U346.
N Z Med J. 2003 Jan 24;116(1168):U291.
N Z Med J. 2003 Mar 14;116(1170):U368.
N Z Med J. 2003 Mar 14;116(1170):U375.

Ischaemic heart disease, Type 1 diabetes, and cow milk A1 beta-casein.

Laugesen M, Elliott R.

Health New Zealand, Auckland, New Zealand. laugesen@healthnz.co.nz

AIM: To test the correlation of per capita A1 beta-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 beta-casein content (A1/beta) (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. 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/beta in milk and cream (r = 0.47, p <0.05). Correlations were not significant for A2, B or C variants of milk beta-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 beta-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 beta-casein/capita. Surveys of A1 beta-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.
Darauf antwortet ein gewisser Hill unter anderem:

The paper by Laugesen and Elliott 1 published recently in the NZMJ (http://www.nzma.org.nz/journal/116-1168/295/) contains a number of inconsistencies that seriously bring into question its conclusion that consumption of A1-casein has a significant influence on heart disease and Type 1 diabetes.

As with any epidemiological study, all that this paper demonstrates is a relationship and not cause and effect. In the absence of other information, at best it provides a starting point for further research targeted at establishing true cause and effect. (...)

Type 1 diabetes

The reference to the feeding trials and particularly the paper by Beales et al, does not mention that the main conclusion from the trials was that milk-based diets, including the A1-casein diet, were protective against diabetes compared with a milk-free, wheat-predominant diet, which was highly diabetogenic. (...)
The fact that the inclusion of the B and C variants of beta-casein in the analysis weakened the relationship between milk consumption and the incidence of Type 1 diabetes is very difficult to explain mechanistically.

The inclusion of cheese also weakened the relationship between milk consumption and the incidence of Type 1 diabetes. Again, as most cheeses contain a significant amount of A1-casein, from a mechanistic perspective it is difficult to explain why this should be the case. Based on our understanding of dairy chemistry, the inclusion of cheese should strengthen and not weaken the relationship. As Laugesen and Elliott themselves state, A1 consumption has been declining across 17 of the countries they analysed, yet the incidence of diabetes has been increasing markedly. Therefore, other factors must be responsible for the marked increase in Type 1 diabetes in children.

Ischaemic heart disease

One of the main criticisms of this work, as mentioned by Laugesen and Elliott, is that the authors could find no relationship between the consumption of tobacco and deaths due to heart disease, when this is already known to be a significant risk factor. The lack of a correlation with tobacco consumption very much highlights the dangers of relying on epidemiological data as evidence of cause and effect.

The authors have used deaths due to heart disease and not the incidence of the disease in their correlations. Using data on forty countries, we have recently completed work looking at the relationship between heart disease and the consumption of a whole range of foods. As we believe it is not valid to subject these data to a number of unsubstantiated manipulations in order to provide a value for A1-casein consumption, we used milk protein.3 In doing so, we made the assumption that if there was something in milk protein, such as A1-casein, that was strongly associated with the induction of diseases, then by using data from enough countries we would expect to see a significant relationship between disease and the per capita consumption of milk protein. In our analysis we found that milk protein was correlated with neither deaths due to heart disease nor the non-fatal incidence of heart disease.
Die Diskussion geht dann noch weiter - das erspare ich mir mal. Mein Fazit hierzu: Alles noch ziemlich spekulativ.