Stavia, real goat's milk feta is very difficult for me to find, but would be an enormous treat
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Thanks to all for your wonderful leads that led me down a rabbit's hole last night. I needed to understand the mechanism to buy into this A1/A2 hypothesis. From what I’ve learned, A1 milk has a switch with a single peptide at the 67th position; histadine rather than proline. Histadine renders the protein unstable during hydrolysis and little protein fragment called beta-casomorphin7 (BCM7) results. BCM7, an opiod receptor, can apparently get into the blood stream and into the brain where it binds with opiod receptors. It is correlated with autism, schizophrenia, CVD, and diabetes. Interestingly, in mice studies when naxalone (which prevents the opiod binding) is administered with A1 milk, the negative health consequences completely DISAPPEAR.
No negative health consequences have been associated with A2 milk. None. Here's a good
summary of the health effects from A1 and A2 dairy on humans:
BCM7 is suggested to be associated as a risk factor for human health hazards as it can potentially affect numerous opioid receptors in the nervous, endocrine and immune system. It is also known to be an oxidant of low dietary lipoproteins (LDL) and oxidation of LDL is believed to be important in formation of arterial plaque. Epidemiological evidences claim that consumption of beta-casein A1 milk is associated as a risk factor for type-1 diabetes, coronary heart disease, arteriosclerosis, sudden infant death syndrome, autism, schizophrenia etc.[3,4] A broad range of studies from American and European investigations has shown reduction in autistic and schizophrenic symptoms with decrease in A1 milk intake.[5] Further, animal trials have also supported the linking of type-1 diabetes to milk exposure in general and A1 beta-casein in particular.
Populations, which consume milk containing high levels of β-casein A2 variant, have a lower incidence of cardiovascular disease and type-1 diabetes. The A1/A2 hypothesis is both intriguing and potentially very important for public health if it is proved correct. It should be taken seriously and deeper research is needed to verify the range and nature of BCM7 interactions with the human gastrointestinal tract and whole organism. This requires more of animal trials and generation of data on human subjects having the problems related to A1/A2 beta-casein milk consumption.
Here’s a study with humans comparing the effect of A1 and A2 milk. It would be very interesting to see the same experiment on folks who don’t report negative symptoms with dairy consumption.
Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ milk
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818854/
Results
Compared with milk containing only A2 β-casein, the consumption of milk containing both β-casein types was associated with significantly greater PD3 symptoms; higher concentrations of inflammation-related biomarkers and β-casomorphin-7; longer gastrointestinal transit times and lower levels of short-chain fatty acids; and increased response time and error rate on the SCIT. Consumption of milk containing both β-casein types was associated with worsening of PD3 symptoms relative to baseline in lactose tolerant and lactose intolerant subjects. Consumption of milk containing only A2 β-casein did not aggravate PD3 symptoms relative to baseline (i.e., after washout of dairy products) in lactose tolerant and intolerant subjects.
Conclusions
Consumption of milk containing A1 β-casein was associated with increased gastrointestinal inflammation, worsening of PD3 symptoms, delayed transit, and decreased cognitive processing speed and accuracy. Because elimination of A1 β-casein attenuated these effects, some symptoms of lactose intolerance may stem from inflammation it triggers, and can be avoided by consuming milk containing only the A2 type of beta casein.