The fact that there are opioid receptors in the gut indicates that opioids play a normal physiological role. Sure, some cows evolved to produce A1, but saying that if nature intended it other animals would make A1 too is bollocks. And since when did nature intend mice to drink cows milk? If anything humans exposed to drinking A1 over thousands of years should have led to development of tolerance in some populations. Populations not exposed to A1 milk until recently (eg Chinese) might logically be expected to have more issues with A1.
BCM-7 produced from the A1 point mutated protein apparently has opioid-like activity and this receptor signalling affects gut motility, hence the symptoms and main selling differential. A2 should keep running with this line, it has proven to be very successful to date! Esp in babies where breast milk is the only source of nutrition. But nothing to do with inflammation and no mechanism for inflammation proposed.
To test for an impact on inflammation in humans where it is relevant you would need to run a trial of pure A2 vs ordinary milk, then do endoscopies and small bowel biopsies to look at inflammation (good luck getting ethics approved), but without any real strategy of what to test for or what the results mean anyway. Money would be better spent focusing on studies confirming symptoms experienced when ingesting A1 vs A2. Far easier to perform and more meaningful to the consumer.
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