So, looking at some stuff today. Regarding diabetes:
This study (PDF) found casein was possibly diabetogenic, but in some cases,
protective:
Quote:
A milk-free, wheat-predominant diet was highly diabetogenic in three widely separate locations in both animal models. A previous result that A1 β-casein was more diabetogenic than A2 β-casein in NOD mice was not confirmed; both β-casein variants were protective in BB rats and NOD
mice. Whole Casein promoted diabetes in NOD/Ba but protected BB showing that unique diabetes haplotypes react differently to dietary proteins. A1- was
more diabetogenic than A2-β-casein only in PS-fed BB rats. Neither the analysis of insulitis nor of pancreatic cytokine gene expression showed a difference between A1 or A2 β-casein fed animals. Milk caseins are
unlikely to be exclusive promoters of Type I diabetes, but could enhance the outcome of diabetes in some cases. Other diet components such as wheat could be more important promoters of Type I diabetes.
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So, wheat appears to have more of an influence, or maybe wheat rat chow.
The 'Critique of Truswell's' thing was a review, and someone sent a letter to the editor about it. None can be viewed without a paid subscription. Here is the
Abstract of what he wrote. I gather from another reference that he didn't feel it held up. It is hard to prove things from vast sweeping epidemiological reviews.
Regarding the Czech cows, that was mostly about how to type cows for what kind of casein-milk they will make. The science they referred to was Elliott's epidemiological reviews around 1999 and McLachlan - McLachlan was inspired by Elliott, basically. The Czech article also said:
Quote:
At present the data related to coronary disease must be viewed as inconclusive. Only one rather limited experiment has been described comparing A1 and A2 β-caseins' effects on coronary heart disease. This experiment has several defects in its design and an inappropriate animal model was used. Further, no mechanism has been presented for any differential effect of cow’s milk β-casein types on the pathogenesis of coronary heart disease.
The evidence relating autism and schizophrenia to A1 or A2 β-caseins in milk is even more speculative, and the evidence is more unsubstantial than that for diabetes mellitus I and for coronary heart disease.
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Here is some McLachlan-related stuff:
This NZ epidemiological review was mixed about A1 (but felt further study was warranted), and later
McLachlan responded to it. Both are a good read. Neither is an actual clinical study, however. And since we always want to know funding and so on, all of that is funded by milk companies, and McLachlan himself started the whole A2 thing and founded the A2 company. Apparently he has passed away.
I couldn't find anything about the Campwell thing in any "Journal of Atherosclerosis" anywhere so far. The studies that supposedly support those findings are a combination of
this abstract of a French study (I haven't found full text) linking the casein to tyrosyl and
this LDL study that discusses a possible role for tyrosyl in LDL formation. It's a bit over my head, so I'm going to leave it aside for now and come back to it (especially if I can find the French thing).
It doesn't seem that major though. There was one study about LDL in rabbits
showing that casein caused hypercholesterolemia (the action having to do with blocking cleaning it out, not creating more). Now, I can't get the full text on this without paying, but apparently
casein does cause hypercholesterolemia in rabbits, but not rats or humans.
Here's an abstract regarding humans.
I want to come back and read this later, it looks like a good primer on opioid peptides:
Neuropharmacology of Endogenous Opioid Peptides.
Also interesting:
Evidence That Intermittent, Excessive Sugar Intake Causes Endogenous Opioid Dependence
Quote:
In summary, an opioid-mediated dependence on sugar has been demonstrated at both the behavioral and neurochemical level. The withdrawal signs observed in this study suggest that dependence on endogenous opioids can develop during the ingestion of very palatable food on some eating schedules.
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So maybe what's addictive is...any food you really enjoy.
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