A2 - A1 Milk Gene story is far too important to ignore

[Guest guest]

It's all about one ittybitty gene, and it's driving me nuts

I know I should not let things get me so upset. After all, it isn't as though there aren't a myriad other irrational, illogical corrupt and asinine public positions taken in the health and food sector - so why should this one get to me more than the others?

Maybe it's because I remember how much drinking milk meant to me as a growing boy. Or it is because I can envision millions upon millions of young children drinking their milk ( for better health) in school cafeterias everywhere. Whatever the reason, the fact that this story is being utterly ignored drives me to distraction. This is an issue that need not be controversial for decades before resolution -- like mercury in our mouths or trans-fatty acids found in billions of supermarket junk products. This issue can be resolved quickly, and it should be -- because we tell our kids to drink their milk every day

The issue is the genetic makeup of everyday cow's milk. Whether that milk is A1 or A2 might make all the difference in the world to chronic disease rates of the future. Apparently it has made a difference in the amount of diabetes, heart disease, autism and other maladies for a long, long time.

We broke the sensational A-2 milk story a year ago in June and followed up with the breaking story of animal research verifying the controversial thesis that A1 milk is unhealthy in July 2003

Then the story suddenly stopped in its tracks, as if drinking milk isn't a major factor in the health of young children. The two main protagonists behind this story in New Zealand died late in 2003. On top of that, the company here in America that purchased the rights to the A2 milk patents has had nothing to say … nothing!

This really, really bugs me. Even the people concerned with organic, raw milk are ignoring A2 milk. Why?

Because there are a lot of costly commercial changes that "all" the dairy industries must make when this genetic milk question gets the attention it deserves.

True Health is resurrecting this important milk controversy because serious health advocates are going to want raw, organic A2 milk -- especially for their children. We continue to be amazed that the major media in America has ignored this important story since it first erupted in the New Zealand and Australian press, and in scientific journals a few years ago

There is new information, thanks to the genes in the Guernsey breed of milk cows. Guernsey are naturally more genetically-capable of producing A2 dominant milk, and both the US and British Guernsey Breeding Associations have begun to sponsor more scientific studies to support the thesis as they genetically test their breeder bulls and herd in order to advertise this advantage

Be prepared to hear the naysayer chants from Holstein and other popular dairy breeds, as well as the modern dairy industry that brought you unsanitary, homogenized pasteurized and inferior products for decades.

Milk is a traditional staple food. It contains about 32 grams of protein per quart and 82% of that protein is casein. Casein is divided into four subclasses with beta-casein as the second most abundant. Scientists have determined 10 genetic characterizations for beta-casein with A1, A2, A3 and B found in virtually all common - Bos taurus - dairy cow populations. In a nutshell the thesis is : A1 milk is bad ; A2 milk is good.

Going back to the beginning, the story started in New Zealand, an island nation with dairy one its major exports. Back in 1991 Dr Bob Elliott, a paediatrician, noticed during clinical visits to the Pacific Islands that children of the islands did not have any Type 1 diabetes. He also noted that dairy cows were not part of the cultures of the islands.

( At True Health we are harkened back to the work of Dr Weston A Price in the 1930s, when he demonstrated conclusively that cultural differences in the diet clearly resulted in basic health differences. The Establishment ignored his work, but `what else is new?' Of course, Dr Price did not have the modern science of genetics working for him )

Dr Elliott took his observations about the lack of diabetes dovetailing with the lack of cow's milk to Dr Hill, chief protein chemist for the old Dairy Board of New Zealand. Hill then suggested that the protein type might be to blame -- A1 beta casein as opposed to A2 beta casein

How Dr Hill knew such a possibility lurked has not been explained

Dr Elliott set out to prove A1 could be a disease cause. With the backing of the Dairy Board and the Child Health Research Foundation, he tested the idea on mice, feeding them either A1 or A2 protein.

None of the animals consuming A2 milk developed diabetes, many in the A1 group did. Elliott and the organizations knew they were on to something. The group filed for the first patents to test cows for A1 and A2 milk producers

However Dr Elliott committed an unpardonable sin in scientific circles … he gave his findings to the media before they were published in the peer-reviewed literature

Naturally the A1 diabetes connection was headlined for several days by the media Down Under, and the Dairy Board was stung by its own research. The eruption of controversy generated defensive dogma in the status quo and the work was happily dismissed by the world-wide industry / academic powers

Enter the late Dr Corrie McLachlan, a scientist whose passion had been heart disease. In 1990, he developed a cholesterol-free butter, but remained unconvinced that cholesterol was the main culprit in heart disease. When he looked at Elliott's diabetes data for the first time in 1994, he exclaimed out loud "If I didn't know better, I'd say I was looking at heart disease."

He then spent about a year and a half collecting data on the two protein types of milk, comparing consumption amounts with disease figures.

One of the epidemiological observations noted by McLachlan, for example, pointed out that Finland has a very high incidence of heart disease and diabetes ; it also has a strong line of Ayrshire cows, which produce mostly A1 milk and very little A2

On the other hand, Iceland features dairy herds with high A2 production and little A1, giving the people a very high A2 consumption -- Iceland has virtually no heart disease nor diabetes!

McLachlan lodged his own patent for testing A2 milk, then asked the Dairy Board for more funding to continue research

Then confusion of the kind peculiar to peer-reviewed scientific circles reared its confounding head. Appearing much like today's confused and agenda-driven science in other areas, such as into health implications of mercury amalgam fillings or microwave radiation and mobile phones, the verification process ran into snags and controversy

Interestingly, none of this news managed to stir the managed American media

The Dairy Board arranged for international studies to replicate Elliott's initial diabetes work. The studies proved nothing. A Canadian animal study supported Elliott's work ; Britain's study did not, and Elliott's own replication saw mice die of infections, spoiling any result. This is not at all unusual in scientific research. A summary of the fiasco suggests that mistakes in animal handling and changes in diets confused everything

Funding dried up without scientific resolutions. It was alleged that the Dairy Board had adopted an attitude. They wanted to simply leave well enough alone. The board denied it, and pointed to their filing of a new patent covering a test for identifying people susceptible to juvenile diabetes. ( No news has generated from this fact either.)

Ticky Fullerton, a capable Australian television interviewer summarized the case well :

"Just who would be susceptible to A1 milk was open to question. The hypothesis pointed to those with low immunity, but often this goes undetected. Nevertheless, a possible mechanism for how A1 milk might cause disease was proposed. Protein molecules of A1 and A2 milk are both chains of amino acids. But in the A1 molecule, one amino acid is different, a weak link. A2 researchers believed this causes the chain to break, creating a small piece called beta-casomorphin-7. And this piece is able to move through the gut wall in to the blood, triggering disease, That idea fuelled the hypothesis …"

Internationally, immunologists balked -- claiming the data was insufficient to prove the thesis. Stalling thus occurred on the research front.

Meanwhile, Dr McLachlan sold much of his valuable collection of rare books and borrowed from his family to keep his heart disease connection going.

"The data was too good," he said. "I'm pretty good at research, and my guess was that the data was correct. I figured if I didn't keep going, it would be buried forever and you wouldn't see it"

Along came the late Paterson, a dairyman with the kind of money to realize the potential in the face of strong, dogmatic opposition. Paterson noted not only the money-making potential, but he saw "a genuine moral imperative to do what is correct." ( It would be nice if that moral imperative had more legs with today's establishment.)

Despite " a lot of Machiavellian stuff" Paterson, McLachlan and A2 Corporation managed to purchase half the patent protection from the old Dairy Board and combine it with new business parameters well enough to get on the stock market and cause a brief flurry.

This still wasn't important enough news for the major media

The corporate plan is for farmers to pay $20 for a cow DNA test to determine A1 or A2, and the company anticipated a royalty on every glass of A2 milk sold henceforth

However both McLachlan and Paterson died late in 2003, and their driving forces seemed to die with them. A2 Corporation in New Zealand is no longer responding to emails and phone calls

Last year, Professor , a noted Vascular Biologist at the University of Queensland, Australia used rabbits as test animals and found "Highly significant" results. The animals fed A1 developed much higher serum cholesterol levels than those fed A2

On television Dr said :

"we found that the A1 made the juvenile fatty streaks, the ones you get in children, much worse. So it may be important the type of milk that children drink ; whether it has A1 or A2 casein. However, by the time you are an adult, it's not going to affect you whether you drink one or the other, but the damage may have been done in childhood."

Her opinion on adult affects was merely an opinon. Whether adults are affected less than children is not supported by any science at this time.

Dr 's published study should have been major news worldwide. Of all the media, only True Health told the story -- in our July-August 2003 issue. The following additional information was gleaned from that story:

The particular genetic version of A1 is found in the majority of western civilization's cows with Holstein and Ayrshire breeds producing 63% and 67% A1 respectively, leaving 35% and 33% of the casein the A2 variety.

The differences between A1 and A2 protein is very slight, showing up in a single amino acid in the long chain. Genetic research has determined that the only difference is on condon 67 where A2 has the amino acid proline and A1 has the amino acid histadine. This single amino-acid sequence differential appears to be significant in living mammal biology

Researchers in Australia explained the possible mechanism whereby A1 is detrimental while A2 is beneficial.

"What are the possible mechanisms by which the different casein variants affect the development of atherosclerosis? Firstly, there is the effect of beta-casein A2 on lowering serum cholesterol. Secondly, beta-casein A1 and not A2, releases beta-casomorphin-7, which is thought to be involved in the oxidation of LDL cholesterol through a peroxides-dependent process. Beta-casomorphins have been detected in the plasma of newborn calves and in the small intestines of humans after cow milk consumption …"

In technical language the paper further explains that an enzyme called elastase releases the carboxyl terminus of beta-casomorphin-7 between the 66 and 67 ( histadine) positions on the chain of amino acids as they are found on the A1 protein. Elastoase is unable to cleave the bond at the same position on the A2 protein, which means the beta-Casomorphin-7 cannot be released. The paper then references studies showing how the beta-Casomorphin-7 is implicated in arterial lesions and LDL oxidation.

Additionally the researchers found during the study that A1 appears to enhance opportunity for chronic inflammation in arteries, which is a known risk factor for heart disease.

Epidemiological studies conducted by Dr McLachlan were cited in the paper. He had found a correlation between A1 milk consumption and ischemic heart disease in West Germany to be three times greater that the correlation between smoking and ischemic heart disease

Conversely, the populations of Masai and Samburu peoples of Africa, whose diet is chiefly milk and meat from Zebu cattle are virtually free of ischemic heart disease. The African Zebu variety - Bos indicus - produce almost entirely A2 milk.

The study authors concluded :

"These measures ( removing A1 producers ) may thus contribute to improved human health by reducing a risk factor that contributes to ischemic heart disease, the leading cause of premature death in the developed world today"

Now that is news!

Meanwhile, a similar trial using mice instead of rabbits, showed the opposite effect -- A2-fed animals seemed to show slightly larger areas of lesions. So, while mice were significantly affected in a diabetes trial, in this heart disease trial researchers found an opposite situation

However it is know that mice do not naturally get the heart disease, and in the trials they were fed an extremely high-fat diet, which may have masked the protein results. Nevertheless, the test was hailed by fearful status quo hopefuls as a strike against the A2 thesis ( with the entire controversy still managing to avoid media coverage)

The good news is : the Guernsey Cattle Federation sees a tremendous breeding opportunity worldwide, especially in the export of semen to breeders. True Health recently contacted both the English Guernsey Cattle Society and the American Guernsey association

Digby Gribble of the English group said a study is planned which will test the hypothesis that A1 milk may contribute to Autism while A2 milk does not. This study is to be under the guidance of Professor Brotstoff of King's College Hospital, London. Gribble told us :

"He proposes to monitor proteins excreted in the urine of 20 Autistic children. These children will be on casein-free diets already as this is the normal practice on diagnosis of Autism. These children will be on casein-free diets already as this is the normal practice on diagnosis of Autism. They will then be given A2 Guernsey milk from a herd that have all been tested and any cows not A2xA2 will have been removed.

"The proteins in the urine will be measured again and if, as we expect, there are no side effects, then the trial will be repeated with "ordinary" milk which will be a mix of A1 and A2. If the theory that A1 is the trigger then this should show in the urine and in the behaviour of the children"

Gribble explained that the autism project was selected because results will be determined in relatively short order, whereas diabetes and heart disease require long-term verification

The Guernsey breed has been tested in the US and the UK to produce milk that is more than 90% A2, the Breed Societies are testing all bulls used in Artificial Insemination and are making the beta-casein status known to breeders

"In the UK we will no longer use bulls that have tested A1xA1 in artificial insemination and will move to only A2xA2 as soon as we are able. At this time, only the New Zealand Dairy board have tested and published the test results for all of their bulls."

Seth of the American Guernsey Association reported :

"The A2 issue was the topic of much discussion at the annual convention in July, and we have received many requests about A2 as it finally seems not be registering on the radar of the North Americans. Our research and education foundation, the Guernsey Foundation, approved funding for testing of cows in various regions of the US in the next few months."

He added that the association expects to get an accurate picture of where the US Guernsey population stands regarding A2 genetics within a short time. He said he hopes the US Guernsey herds will be able to provide an A2 milk product as the market for it opens up.

Still no major media coverage

By Tom Valentine

[Guest guest]

So how can dairy cow owners test for this?

I'm interested and have been told I can get the test off the internet

for $20, but where?

It's gotta be around somewhere if the Guernsey association is doing

it, right?

>

>

> It's all about one ittybitty gene, and it's driving me nuts

>

> I know I should not let things get me so upset. After all, it isn't

> as though there aren't a myriad other irrational, illogical corrupt

> and asinine public positions taken in the health and food sector -

so

> why should this one get to me more than the others?

>

> Maybe it's because I remember how much drinking milk meant to me as

> a growing boy. Or it is because I can envision millions upon

millions of

> young children drinking their milk ( for better health) in school

> cafeterias everywhere. Whatever the reason, the fact that this

story is

> being utterly ignored drives me to distraction. This is an issue

that

> need not be controversial for decades before resolution -- like

mercury

> in our mouths or trans-fatty acids found in billions of supermarket

junk

> products. This issue can be resolved quickly, and it should be --

> because we tell our kids to drink their milk every day

>

> The issue is the genetic makeup of everyday cow's milk. Whether that

> milk is A1 or A2 might make all the difference in the world to

chronic

> disease rates of the future. Apparently it has made a difference in

the

> amount of diabetes, heart disease, autism and other maladies for a

long,

> long time.

>

> We broke the sensational A-2 milk story a year ago in June and

followed

> up with the breaking story of animal research verifying the

> controversial thesis that A1 milk is unhealthy in July 2003

>

> Then the story suddenly stopped in its tracks, as if drinking milk

> isn't a major factor in the health of young children. The two main

> protagonists behind this story in New Zealand died late in 2003. On

top

> of that, the company here in America that purchased the rights to

the A2

> milk patents has had nothing to say … nothing!

>

> This really, really bugs me. Even the people concerned with

organic, raw

> milk are ignoring A2 milk. Why?

>

> Because there are a lot of costly commercial changes that " all "

> the dairy industries must make when this genetic milk question gets

the

> attention it deserves.

>

> True Health is resurrecting this important milk controversy because

> serious health advocates are going to want raw, organic A2 milk --

> especially for their children. We continue to be amazed that the

major

> media in America has ignored this important story since it first

erupted

> in the New Zealand and Australian press, and in scientific journals

a

> few years ago

>

> There is new information, thanks to the genes in the Guernsey breed

of

> milk cows. Guernsey are naturally more genetically-capable of

producing

> A2 dominant milk, and both the US and British Guernsey Breeding

> Associations have begun to sponsor more scientific studies to

support

> the thesis as they genetically test their breeder bulls and herd in

> order to advertise this advantage

>

> Be prepared to hear the naysayer chants from Holstein and other

popular

> dairy breeds, as well as the modern dairy industry that brought you

> unsanitary, homogenized pasteurized and inferior products for

decades.

>

> Milk is a traditional staple food. It contains about 32 grams of

protein

> per quart and 82% of that protein is casein. Casein is divided into

four

> subclasses with beta-casein as the second most abundant. Scientists

have

> determined 10 genetic characterizations for beta-casein with A1,

A2, A3

> and B found in virtually all common - Bos taurus - dairy cow

> populations. In a nutshell the thesis is : A1 milk is bad ; A2 milk

is

> good.

>

> Going back to the beginning, the story started in New Zealand, an

island

> nation with dairy one its major exports. Back in 1991 Dr Bob

Elliott, a

> paediatrician, noticed during clinical visits to the Pacific Islands

> that children of the islands did not have any Type 1 diabetes. He

also

> noted that dairy cows were not part of the cultures of the islands.

>

> ( At True Health we are harkened back to the work of Dr Weston A

Price

> in the 1930s, when he demonstrated conclusively that cultural

> differences in the diet clearly resulted in basic health

differences.

> The Establishment ignored his work, but `what else is new?' Of

> course, Dr Price did not have the modern science of genetics

working for

> him )

>

> Dr Elliott took his observations about the lack of diabetes

dovetailing

> with the lack of cow's milk to Dr Hill, chief protein chemist

> for the old Dairy Board of New Zealand. Hill then suggested that the

> protein type might be to blame -- A1 beta casein as opposed to A2

beta

> casein

>

> How Dr Hill knew such a possibility lurked has not been explained

>

> Dr Elliott set out to prove A1 could be a disease cause. With the

> backing of the Dairy Board and the Child Health Research

Foundation, he

> tested the idea on mice, feeding them either A1 or A2 protein.

>

> None of the animals consuming A2 milk developed diabetes, many in

the A1

> group did. Elliott and the organizations knew they were on to

something.

> The group filed for the first patents to test cows for A1 and A2

milk

> producers

>

> However Dr Elliott committed an unpardonable sin in scientific

circles

> … he gave his findings to the media before they were published in

> the peer-reviewed literature

>

> Naturally the A1 diabetes connection was headlined for several days

by

> the media Down Under, and the Dairy Board was stung by its own

research.

> The eruption of controversy generated defensive dogma in the status

quo

> and the work was happily dismissed by the world-wide industry /

academic

> powers

>

> Enter the late Dr Corrie McLachlan, a scientist whose passion had

been

> heart disease. In 1990, he developed a cholesterol-free butter, but

> remained unconvinced that cholesterol was the main culprit in heart

> disease. When he looked at Elliott's diabetes data for the first

> time in 1994, he exclaimed out loud " If I didn't know better,

> I'd say I was looking at heart disease. "

>

> He then spent about a year and a half collecting data on the two

protein

> types of milk, comparing consumption amounts with disease figures.

>

> One of the epidemiological observations noted by McLachlan, for

example,

> pointed out that Finland has a very high incidence of heart disease

and

> diabetes ; it also has a strong line of Ayrshire cows, which produce

> mostly A1 milk and very little A2

>

> On the other hand, Iceland features dairy herds with high A2

production

> and little A1, giving the people a very high A2 consumption --

Iceland

> has virtually no heart disease nor diabetes!

>

> McLachlan lodged his own patent for testing A2 milk, then asked the

> Dairy Board for more funding to continue research

>

> Then confusion of the kind peculiar to peer-reviewed scientific

circles

> reared its confounding head. Appearing much like today's confused

> and agenda-driven science in other areas, such as into health

> implications of mercury amalgam fillings or microwave radiation and

> mobile phones, the verification process ran into snags and

controversy

>

> Interestingly, none of this news managed to stir the managed

American

> media

>

> The Dairy Board arranged for international studies to replicate

> Elliott's initial diabetes work. The studies proved nothing. A

> Canadian animal study supported Elliott's work ; Britain's study

> did not, and Elliott's own replication saw mice die of infections,

> spoiling any result. This is not at all unusual in scientific

research.

> A summary of the fiasco suggests that mistakes in animal handling

and

> changes in diets confused everything

>

> Funding dried up without scientific resolutions. It was alleged

that the

> Dairy Board had adopted an attitude. They wanted to simply leave

well

> enough alone. The board denied it, and pointed to their filing of a

new

> patent covering a test for identifying people susceptible to

juvenile

> diabetes. ( No news has generated from this fact either.)

>

> Ticky Fullerton, a capable Australian television interviewer

summarized

> the case well :

>

> " Just who would be susceptible to A1 milk was open to question. The

> hypothesis pointed to those with low immunity, but often this goes

> undetected. Nevertheless, a possible mechanism for how A1 milk might

> cause disease was proposed. Protein molecules of A1 and A2 milk are

both

> chains of amino acids. But in the A1 molecule, one amino acid is

> different, a weak link. A2 researchers believed this causes the

chain to

> break, creating a small piece called beta-casomorphin-7. And this

piece

> is able to move through the gut wall in to the blood, triggering

> disease, That idea fuelled the hypothesis … "

>

> Internationally, immunologists balked -- claiming the data was

> insufficient to prove the thesis. Stalling thus occurred on the

research

> front.

>

> Meanwhile, Dr McLachlan sold much of his valuable collection of rare

> books and borrowed from his family to keep his heart disease

connection

> going.

>

> " The data was too good, " he said. " I'm pretty good at

> research, and my guess was that the data was correct. I figured if I

> didn't keep going, it would be buried forever and you wouldn't

> see it "

>

> Along came the late Paterson, a dairyman with the kind of

money

> to realize the potential in the face of strong, dogmatic opposition.

> Paterson noted not only the money-making potential, but he saw " a

> genuine moral imperative to do what is correct. " ( It would be nice

> if that moral imperative had more legs with today's establishment.)

>

> Despite " a lot of Machiavellian stuff " Paterson, McLachlan and

> A2 Corporation managed to purchase half the patent protection from

the

> old Dairy Board and combine it with new business parameters well

enough

> to get on the stock market and cause a brief flurry.

>

> This still wasn't important enough news for the major media

>

> The corporate plan is for farmers to pay $20 for a cow DNA test to

> determine A1 or A2, and the company anticipated a royalty on every

glass

> of A2 milk sold henceforth

>

> However both McLachlan and Paterson died late in 2003, and their

driving

> forces seemed to die with them. A2 Corporation in New Zealand is no

> longer responding to emails and phone calls

>

> Last year, Professor , a noted Vascular Biologist at

the

> University of Queensland, Australia used rabbits as test animals and

> found " Highly significant " results. The animals fed A1 developed

> much higher serum cholesterol levels than those fed A2

>

> On television Dr said :

>

> " we found that the A1 made the juvenile fatty streaks, the ones you

> get in children, much worse. So it may be important the type of milk

> that children drink ; whether it has A1 or A2 casein. However, by

the

> time you are an adult, it's not going to affect you whether you

> drink one or the other, but the damage may have been done in

> childhood. "

>

> Her opinion on adult affects was merely an opinon. Whether adults

are

> affected less than children is not supported by any science at this

> time.

>

> Dr 's published study should have been major news worldwide.

> Of all the media, only True Health told the story -- in our July-

August

> 2003 issue. The following additional information was gleaned from

that

> story:

>

> The particular genetic version of A1 is found in the majority of

western

> civilization's cows with Holstein and Ayrshire breeds producing 63%

> and 67% A1 respectively, leaving 35% and 33% of the casein the A2

> variety.

>

> The differences between A1 and A2 protein is very slight, showing

up in

> a single amino acid in the long chain. Genetic research has

determined

> that the only difference is on condon 67 where A2 has the amino acid

> proline and A1 has the amino acid histadine. This single amino-acid

> sequence differential appears to be significant in living mammal

biology

>

> Researchers in Australia explained the possible mechanism whereby

A1 is

> detrimental while A2 is beneficial.

>

> " What are the possible mechanisms by which the different casein

> variants affect the development of atherosclerosis? Firstly, there

is

> the effect of beta-casein A2 on lowering serum cholesterol.

Secondly,

> beta-casein A1 and not A2, releases beta-casomorphin-7, which is

thought

> to be involved in the oxidation of LDL cholesterol through a

> peroxides-dependent process. Beta-casomorphins have been detected

in the

> plasma of newborn calves and in the small intestines of humans

after cow

> milk consumption … "

>

> In technical language the paper further explains that an enzyme

called

> elastase releases the carboxyl terminus of beta-casomorphin-7

between

> the 66 and 67 ( histadine) positions on the chain of amino acids as

they

> are found on the A1 protein. Elastoase is unable to cleave the bond

at

> the same position on the A2 protein, which means the beta-

Casomorphin-7

> cannot be released. The paper then references studies showing how

the

> beta-Casomorphin-7 is implicated in arterial lesions and LDL

oxidation.

>

> Additionally the researchers found during the study that A1 appears

to

> enhance opportunity for chronic inflammation in arteries, which is a

> known risk factor for heart disease.

>

> Epidemiological studies conducted by Dr McLachlan were cited in the

> paper. He had found a correlation between A1 milk consumption and

> ischemic heart disease in West Germany to be three times greater

that

> the correlation between smoking and ischemic heart disease

>

> Conversely, the populations of Masai and Samburu peoples of Africa,

> whose diet is chiefly milk and meat from Zebu cattle are virtually

free

> of ischemic heart disease. The African Zebu variety - Bos indicus -

> produce almost entirely A2 milk.

>

> The study authors concluded :

>

> " These measures ( removing A1 producers ) may thus contribute to

> improved human health by reducing a risk factor that contributes to

> ischemic heart disease, the leading cause of premature death in the

> developed world today "

>

> Now that is news!

>

> Meanwhile, a similar trial using mice instead of rabbits, showed the

> opposite effect -- A2-fed animals seemed to show slightly larger

areas

> of lesions. So, while mice were significantly affected in a diabetes

> trial, in this heart disease trial researchers found an opposite

> situation

>

> However it is know that mice do not naturally get the heart

disease, and

> in the trials they were fed an extremely high-fat diet, which may

have

> masked the protein results. Nevertheless, the test was hailed by

fearful

> status quo hopefuls as a strike against the A2 thesis ( with the

entire

> controversy still managing to avoid media coverage)

>

> The good news is : the Guernsey Cattle Federation sees a tremendous

> breeding opportunity worldwide, especially in the export of semen to

> breeders. True Health recently contacted both the English Guernsey

> Cattle Society and the American Guernsey association

>

> Digby Gribble of the English group said a study is planned which

will

> test the hypothesis that A1 milk may contribute to Autism while A2

milk

> does not. This study is to be under the guidance of Professor

Brotstoff

> of King's College Hospital, London. Gribble told us :

>

> " He proposes to monitor proteins excreted in the urine of 20

> Autistic children. These children will be on casein-free diets

already

> as this is the normal practice on diagnosis of Autism. These

children

> will be on casein-free diets already as this is the normal practice

on

> diagnosis of Autism. They will then be given A2 Guernsey milk from a

> herd that have all been tested and any cows not A2xA2 will have been

> removed.

>

> " The proteins in the urine will be measured again and if, as we

> expect, there are no side effects, then the trial will be repeated

with

> " ordinary " milk which will be a mix of A1 and A2. If the theory

> that A1 is the trigger then this should show in the urine and in the

> behaviour of the children "

>

> Gribble explained that the autism project was selected because

results

> will be determined in relatively short order, whereas diabetes and

heart

> disease require long-term verification

>

> The Guernsey breed has been tested in the US and the UK to produce

milk

> that is more than 90% A2, the Breed Societies are testing all bulls

used

> in Artificial Insemination and are making the beta-casein status

known

> to breeders

>

> " In the UK we will no longer use bulls that have tested A1xA1 in

> artificial insemination and will move to only A2xA2 as soon as we

are

> able. At this time, only the New Zealand Dairy board have tested and

> published the test results for all of their bulls. "

>

> Seth of the American Guernsey Association reported :

>

> " The A2 issue was the topic of much discussion at the annual

> convention in July, and we have received many requests about A2 as

it

> finally seems not be registering on the radar of the North

Americans.

> Our research and education foundation, the Guernsey Foundation,

approved

> funding for testing of cows in various regions of the US in the

next few

> months. "

>

> He added that the association expects to get an accurate picture of

> where the US Guernsey population stands regarding A2 genetics

within a

> short time. He said he hopes the US Guernsey herds will be able to

> provide an A2 milk product as the market for it opens up.

>

> Still no major media coverage

>

> By Tom Valentine

>

[Guest guest]

Thanks. Gordon. I had never read that about A2 milk before. Guess

you learn something everyday!!! I did a search and found a site that said,

jersey cows, sheep, goats and buffalo were also A2 producers. Thanks again.

This puts another piece in the nutrient puzzle for me.

http://hillhousewriters.com

[Guest guest]

Can you share the link?

Debbie ChikouskyManitoba, Canadagdchik@..."The person who wants something will find a way. The person who doesn’t will find an excuse."

Re:A2 - A1 Milk Gene story is far too important to ignore

Thanks. Gordon. I had never read that about A2 milk before. Guess you learn something everyday!!! I did a search and found a site that said, jersey cows, sheep, goats and buffalo were also A2 producers. Thanks again. This puts another piece in the nutrient puzzle for me.

http://hillhousewriters.com

[Guest guest]

Ms. W,

My reading plus the test results I received tell me that the Jersey breed is not an automatic A2 producer. Jerseys are subject to the same probabilities as other dairy breeds. What keeps sheep and goats safe from the A1 intrusion is the inability of these species to breed with Bos Taurus. So far, A1 hasn't been found in Bos Indicus cattle. I read that they have a different number of chromosomes than Bos Taurus and this was held responsible for the A1 not transferring to them.

I know that buffalo are commonly cross bred with Bos Taurus cattle. I would suspect that they might acquire the A1 from a Bos Taurus that carried it.

The only way that I'm aware of to determine whether a particular animal carried the A1 is by DNA testing. Since the holders of the patent to administer the test has so far restricted it's use of the test to commercial dairy herds, I would be reluctant to accept any statement that any entire breed of Bos Taurus were A2 producers. A1 prevalence in commercial herds was as high as 70%.

One herd in particular reportedly tested 1500 cows. around 500 were positive for A2, but only 175 were suitable for the pure A2 herd. This leads me to believe that 500 tested positive for A2, but only 175 tested homozygous for it. Those 175 would be the only ones that would produce pure A2 milk.

The document I received with my test results coded on it consisted of carefully selected cattle from several breeds, including Jersey. It had 23 animals listed. 7 of the animals were AC, meaning one gene for A2, one gene for A1. CC is the code for having both genes for A2. 30% of that batch of samples were not CC. The animals were coded, so I can't be sure which breeds were which, except for my Dexters. 8 were mine, and 6 of them were CC, 2 were AC. The remaining 15, including Jerseys, had 33% carrying A1.

As I said, these cattle were carefully selected for being likely to test positive for A2. The percentages of the general population of cattle that carry A1 is likely much higher. The closer they are to being a mainstream commercial dairy breed, the higher the probability that they will carry A1.

It was my assumption prior to the tests that all American Dexters would test CC for A2 milk unless they could be traced back to an intrusion from another breed. Yet that was not the case. Nowhere in the pedigree of either of my AC animals is there any evidence or suspicion of outcrossing.

One opinion I read guessed that the origin of A1 milk in cattle predates the establishment of many of our modern breeds, including all the British breeds. So the A1 genes would be found in every breed.

The theory I read that makes the most sense to me is that the A1 gene is also tied into another trait that is desirable among dairy cattle. Maybe it helps make good udders or boosts production. This is why it is more prevalent in commercial dairy cattle. It was selected for, inadvertently.

Genebo

Paradise Farm

Re:A2 - A1 Milk Gene story is far too important to ignore

Thanks. Gordon. I had never read that about A2 milk before. Guess you learn something everyday!!! I did a search and found a site that said, jersey cows, sheep, goats and buffalo were also A2 producers. Thanks again. This puts another piece in the nutrient puzzle for me.

http://hillhousewriters.com