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Yeah sorry didn't mean to imply that france doesn't also use Holsteins. Starting in the 30-40's their was mass overbreeding done using genetics which resulted in single cows sometimes birthing 40-100k worth of new cows. At some point during this, a large portion of the offspring switched over t0 producing a1 milk. france & india were the only countries that did not do this type of practice. so the Holstein cattle in those countries are considered heritage of the domesticated kind.Ok thanks, the French countryside did look like it had mostly holstein cows with some others too, but I've not been everywhere and didn't pay so much attention to a1 vs a2 landscapes at the time.
I have found the fortification to be far more of an issue than A1 or A2
It's not that it digests better, but that it feels lighter and gives me no "brain fog" symptoms afterward. You'd only know if the carton told you it was. I think sheep and goats are also free of A1, but need to double check.Can I ask for some updated user experiences with A2 milk? Does it digest better and how would I know if the milk I purchase is A1 or A2? Thank you
I doubt it, I'm sure holstein production is popular everywhere due to the quantity advantage.cow dairy produced in france & india (possibly swiss & italy, to a lesser degree) will be a2
By the incredible Keith Woodford:
A1 beta-casein, type 1 diabetes and links to other modern illnesses
"The scientist who deserves great credit for the initial work and key insights relating to A1 beta-casein and Type 1 diabetes is clearly Professor Bob Elliott, who is with us today as a commentator on this paper. Bob Elliott knew from his work in Samoa that there was a more than 10 fold difference in the incidence of Type 1 diabetes in Samoan children living in New Zealand compared to Samoan children living in Samoa. It was obvious that the factor had to be environmental. Bob Elliott also knew that Samoan children in Samoa drank very much less milk than Samoan children in New Zealand, and milk therefore stood out as an obvious candidate. In addition, Bob Elliott also knew from his own previously published work that casein, or an unidentified component thereof, was diabetogenic in rodents.[5] However, he also knew that the Masai people in Kenya drink large amounts of milk but that childhood diabetes is extremely rare amongst those who still live this traditional lifestyle. In 1993 he therefore approached the NZ Dairy Research Institute, asked to speak to a milk biochemist, and asked the key insightful question: Are there any protein differences in the milk that the Masai people drink compared to the milk that is drunk in New Zealand? The answer, from NZDRI scientist Dr Jeremy Hill, was that there is indeed a difference in the beta casein protein. The milk the Masai people were drinking contained beta casein that was totally A2 whereas that drunk in NZ contained major amounts of the A1 beta casein. It was that question and response that first led to the hypothesis that A1 beta-casein might be implicated in Type 1 diabetes, although at that stage the mechanisms by which it might be occurring were totally unclear. Indeed Jeremy Hill has subsequently said that he always saw it as a ‘long shot’.[6]"
"One of the first steps in testing the hypothesis was to undertake trials with rodents (this time NOD mice). The trials were funded by the New Zealand Dairy Board and the National Children’s Health Research Foundation (a Rotary Charity). The mice were fed a range of diets, including A1 beta-casein, A2 beta casein, or a combination of the two. The results showed that 47% of those fed A1 beta-casein developed Type 1 diabetes whereas none of those fed A2 beta-casein developed diabetes. In another group fed a milk formula containing both A1 and A2 casein there was an intermediate 19% level of diabetes. The differences between the A1 and A2 diets were very highly significant (p<0.001). This indicates that the chance of falsely getting a result like this when there is no underlying cause is less than 1 in 1000. Supplying naloxone (an opioid antagonist) in the drinking water of another group of animals fed A1 beta-casein prevented development of diabetes."
"I would not want [the] debate about A1 beta-casein versus latitude to be taken as an inference that Vitamin D is not relevant to Type 1 diabetes. Almost certainly Type 1 diabetes is a multi-factorial disease, and I therefore remain very open to the notion that Vitamin D is an important part of the overall story. In particular, I note that there is evidence that Type 1 diabetes typically reaches the clinical stage during winter when UV radiation is lowest, and also that diabetics may have lower circulating levels of vitamin D in their bloodstream.[14] But what I do say very strongly, is that neither latitude nor sunlight exposure can be used to explain away the relationships that we have between Type 1 diabetes incidence and intake of A1 beta-casein."
"BCM7 is particularly stable on account of three of its seven amino acids being prolines. However, it is evident that BCM7 can be degraded by the enzyme dipeptidyl peptidase 4 (DPP4) that is found on cell surfaces within mesenteric tissues.[22] It is also apparent that in many people the intestinal lining combined with the presence of DPP4 is sufficient to prevent the BCM7 from passing through in to the bloodstream. However, there is also evidence that in people who for a range of reasons have ‘leaky guts’ it is possible for BCM7 to pass through.[23,24]"
"There are many reasons why individuals can suffer from leaky guts. Newborn babies have permeable intestines to allow macro molecules in colostrum to pass through. In later life, permeability can arise, either short term or long term, from a range of health conditions such as Coeliac disease, ulcerative colitis, Crohn’s disease, and stomach ulcers. Of particular relevance in relation to stomach ulcers is that the historical treatment of ulcers with a high milk diet (such as the Sippy and similar diets) was shown to lead to a very high death rate from heart disease relative to other diets.[25]"
"Bovine BCM7 is a strong opioid.[26,27] It can be counteracted by administration of naloxone but BCM7 has very strong binding affinity and ten times more naloxone is required to counteract a molecule of BCM7 than is required to counteract a molecule of ordinary morphine. Animal trials have shown that in rodents BCM7 easily crosses the blood brain barrier and leads to bizarre behaviour patterns akin to those observed in autism and schizophrenia.[28,29,30] Several groups have shown that autistic humans typically excrete BCM7 in their urine.[31,32,33] This can only have come from milk. Humans milk can also release BCM7 but apparently only in small quantities. Also, human BCM7 is different to bovine BCM7 with the Pro-Gly sequence (positions 4 and 5) replaced by Val-Glu. Human BCM7 is a much weaker opioid than bovine BCM7."
"There is a broad range of evidence suggesting that persons with Type 1 diabetes have enhanced levels of antibodies to beta-casein.[34,35]"
"The epidemiology of heart disease was introduced earlier in this paper. Other evidence relevant to heart disease includes Australian evidence that rodents fed A1 beta casein are susceptible to the development of arterial plaque whereas this does not occur with A2 beta-casein.[44] Also, European research has shown that BCM7 can act as a catalyst in the oxidation of LDL.[45]"
"There are additional autoimmune diseases for which there is existing circumstantial evidence of a link with casein but for which the evidence remains at the hypothesis stage.[46,47,48] The key issue linking many of these autoimmune conditions may be a leaky gut."
"Recently it has also been shown that BCM7 stimulates production of mucins, which are the proteins found within mucus, and which make the mucus sticky.[49] This is consistent with the widely held belief that milk leads to mucus in the throat and nose. It is also apparent, although based on observational evidence and not tested in controlled clinical situations, that a considerable number of people who have previously considered themselves intolerant to milk with symptoms of nausea and diarrhoea, can however drink A2 milk. Indeed it is these experiences that have led many consumers to become A2 believers."
@Blossom @Jennifer (I didn't miss the video, I was just intimidated by those 3 hours)
So you think that the improvement that people notice from switching dairies is purely placenta? No sarcasm.Isn't it weird that most of the research on A1 casein comes from Australia and New Zealand, and that papers from European researchers repeatedly contradict those findings? It's also interesting that almost all of those down Down Under researchers are in one way or another linked to one of those companies that sell miracle A2 milk. Ein Schelm wer sich Böses dabei denkt...
"Disclosure of Interest
As Lincoln University’s Professor of Farm Management and Agribusiness I have close
professional links with all issues affecting the New Zealand dairy industry, and I
undertake significant media commentary on a range of agribusiness issues. I have
undertaken no consultancies for A2 Corporation, Fonterra, or the former NZDRI in
relation to either the issue of A1 and A2 beta-casein, or on any other topic. Prior to June
2007 I had family members who owned a very minor shareholding in A2 Corporation. I
have never personally owned shares on A2 Corporation. The family shares were
purchased on market under normal market conditions. The existence of these family-
owned shares was acknowledged at the time in articles relating to A2 that I wrote. To
avoid any perceptions of direct or indirect interest, and prior to the publication of my
book, my family sold their shares in June 2007."
So you think that the improvement that people notice from switching dairies is purely placenta? No sarcasm.
Oops. But what do you mean by international typo?Was that an intentional typo?
That must be because when people switch from A1- to A2-predominant b-casein, they're only eliminating one potential problem. A2 must still be less problematic in general.What about all the people that don't notice anything? I've tried milk from A2 cow's, and don't feel any difference. Same with sheep's milk cheese such as pecorino vs parmiggiano. I do feel a significant difference when I drink goat's milk. Inspired by the great Travis, I subsitituted all my cow dairy for goat dairy recently, and it definitetly feels better. But as I said, I doubt that the different casein is the main factor, and think that goat's milk is in many other ways superior to cow's milk. Otherwise, I wouldn't be able to explain why I feel no difference with A2 cow's milk (non-homogenized btw) and dairy from sheep.
I milk my own goats and cows. The health of the animal is far more important that ANYTHING else as to the quality of the milk. What they are fed is second and goes back to how healthy the animal is. A healthy cow will clean up crap fed to it, an unhealthy cow will have some pass through.
The individual drinking the milk also has a lot do with digestibility. If you are not digesting it properly, it's a toxin...even if it's supposed to be good for you. I know people do better with one brand of milk over another or raw vs pasteurized and even vice versa. One year, I reacted to one cow's milk but not the other. I know people who can handle A1 milk over A2 milk....probably because of the health of the individual cow. IMO.
A1 or A2 status is way down on the bottom of my list for culling criteria. I won't test my animals. The A2 corporation contract you agree to by testing your animal reads like a Monsanto agreement.
It's not that france & india don't use holstein, they just don't use the breeding techniques the rest of the world uses for cows. It is believed that the mass breeding techniques are responsible for some of the proteins turning into A1. Supposedly all protein from holstein in france & india is A2.It's not that it digests better, but that it feels lighter and gives me no "brain fog" symptoms afterward. You'd only know if the carton told you it was. I think sheep and goats are also free of A1, but need to double check.
I doubt it, I'm sure holstein production is popular everywhere due to the quantity advantage.
just a theory thenIt's not that france & india don't use holstein, they just don't use the breeding techniques the rest of the world uses for cows. It is believed that the mass breeding techniques are responsible for some of the proteins turning into A1. Supposedly all protein from holstein in france & india is A2.
Who do you trust?just a theory then