A1 milk contains A1 beta-casein, which comes from breeds of cows that originated in Northern Europe..

[IGBT]

The controversy between A1 and A2 milk is whether A1 milk causes more inflammation and indigestion than A2 milk.

Some research suggests that A1 milk may cause more inflammation than A2 milk. A recent review of the literature found that A1 milk was linked to upset stomach and inflammation, while A2 milk was not.

However, some say that more research is needed to substantiate this claim.

A1 milk is the most commonly used milk and is obtained from cows of Western origin. A2 milk is obtained from cows of Indian origin.

A1 milk contains A1 beta-casein, which comes from breeds of cows that originated in Northern Europe. Recent research has suggested that milk containing A1 casein can potentially lead to adverse health outcomes including problems with blood sugar and cardiovascular issues.

A2-only milk proponents say that the A1 protein causes indigestion for many people. However, critics say more research is needed to substantiate this claim...
A1 beta-casein is a milk protein that may cause health issues such as:
Type 1 diabetes
Coronary artery disease
Autoimmune disease
Sudden infant death syndrome (SIDS)
Heart disease
Lactose intolerance
Autism
Schizophrenia
A1 beta-casein is digested in the small intestine and produces a peptide called beta-casomorphin-7 (BCM-7). The intestines absorb BCM-7, which then passes into the blood. BCM-7 has inflammatory and immune-disruptive effects on human bodies.
When the body is unable to process A1 beta-casein, it can cause symptoms such as: Digestive problems, Skin rash, Congestion, General fatigue.
A1 beta-casein may also cause stomach discomfort.

 

[GodisanAtheist]

Is @IGBT a bot now?

 

[IGBT]

Hardly...I was studying the health consequences Casein A-1 / A-2 and ran across that body of information. Turns out we are ALL Casein A-1 culpable as per the article.

 

[WelshBloke]

Milk is pretty grim, drink beer instead.

 

[IGBT]

Milk is pretty grim, drink beer instead.

Yes...really good for growing man boobs and shrinking testicles. Sex change in a can...

 

[WelshBloke]

Yes...really good for growing man boobs and shrinking testicles. Sex change in a can...

Ok milk drinker.

 

[DAPUNISHER]

I drink protein shakes with whey isolate and casein. I drink beer too. They must cancel each other out because I'm -

 

[A///]

There's a brand of milk called "a2" here.

 

[WelshBloke]

Yes...really good for growing man boobs and shrinking testicles. Sex change in a can...

Ironically enough...

Hormones in Dairy Foods and Their Impact on Public Health - A Narrative Review Article

The presence of hormones in milk and dairy foods was discussed decades ago but rather more concerns attended to that with respect to finding hormones as biomarkers in milk for diseases and pregnancy diagnosis. Moreover, considerable amount of studies ...

www.ncbi.nlm.nih.gov

 

[mike8675309]

If anyone ever tries to tell you dairy is a healthy food, you can ignore almost whatever they say after that. Childhood dairy intake has been shown to increase the risk of osteoporosis and all sorts of other not-so-good things, and they keep finding more.

 

[IGBT]

This review outlines a hypothesis that A1 one of the common variants of beta-casein, a major protein in cows milk could facilitate the immunological processes that lead to type I diabetes (DM-I). It was subsequently suggested that A1 beta-casein may also be a risk factor for coronary heart disease (CHD), based on between-country correlations of CHD mortality with estimated national consumption of A1 beta-casein in a selected number of developed countries. A company, A2 Corporation was set up in New Zealand in the late 1990s to test cows and market milk in several countries with only the A2 variant of beta-casein, which appeared not to have the disadvantages of A1 beta-casein. https://pubmed.ncbi.nlm.nih.gov/15867940/

 

[Iron Woode]

The controversy between A1 and A2 milk is whether A1 milk causes more inflammation and indigestion than A2 milk.

Some research suggests that A1 milk may cause more inflammation than A2 milk. A recent review of the literature found that A1 milk was linked to upset stomach and inflammation, while A2 milk was not.

However, some say that more research is needed to substantiate this claim.

A1 milk is the most commonly used milk and is obtained from cows of Western origin. A2 milk is obtained from cows of Indian origin.

A1 milk contains A1 beta-casein, which comes from breeds of cows that originated in Northern Europe. Recent research has suggested that milk containing A1 casein can potentially lead to adverse health outcomes including problems with blood sugar and cardiovascular issues.

A2-only milk proponents say that the A1 protein causes indigestion for many people. However, critics say more research is needed to substantiate this claim...
A1 beta-casein is a milk protein that may cause health issues such as:
Type 1 diabetes
Coronary artery disease
Autoimmune disease
Sudden infant death syndrome (SIDS)
Heart disease
Lactose intolerance
Autism
Schizophrenia
A1 beta-casein is digested in the small intestine and produces a peptide called beta-casomorphin-7 (BCM-7). The intestines absorb BCM-7, which then passes into the blood. BCM-7 has inflammatory and immune-disruptive effects on human bodies.
When the body is unable to process A1 beta-casein, it can cause symptoms such as: Digestive problems, Skin rash, Congestion, General fatigue.
A1 beta-casein may also cause stomach discomfort.

I will make this very clear:

Type 1 diabetes is not caused by diet. It is an auto-immune disease.

Many potential environmental triggers have been investigated in large human studies and found to be unassociated with type 1 diabetes risk including duration of breastfeeding, time of introduction of cow milk into the diet, vitamin D consumption, blood levels of active vitamin D, and maternal intake of omega-3 fatty acids.[25][26]

 

[IGBT]

I will make this very clear:

Type 1 diabetes is not caused by diet. It is an auto-immune disease.

No doubt.. once you have Type 1 diabetes what contributing behaviors and diet exasperate the existing condition?? I get the same response from my friends with RA. They believe that it's inherited but fail to understand that diet and behavior can make the suffering plenty worse...they finally ask their doctor the question and they agree..the suffering can get plenty worse if a RA diet is not followed. So off to the dietician to get a "prescription diet" and learn about what foods cause an inflammatory condition thus more "suffering"..

 

[Iron Woode]

No doubt.. once you have Type 1 diabetes what contributing behaviors and diet exasperate the existing condition?? I get the same response from my friends with RA. They believe that it's inherited but fail to understand that diet and behavior can make the suffering plenty worse...they finally ask their doctor the question and they agree..the suffering can get plenty worse if a RA diet is not followed. So off to the dietician to get a "prescription diet" and learn about what foods cause an inflammatory condition thus more "suffering"..

obviously, people must follow dietary and medical advice. This involves insulin injections and choosing carefully what and how much food to eat as well as what physical activities are appropriate.

 

[IGBT]

obviously, people must follow dietary and medical advice. This involves insulin injections and choosing carefully what and how much food to eat as well as what physical activities are appropriate.

Unfortunately for many it isn't obvious or are fully engaged in willful ignorance..too many people with auto-immune conditions participate in their own demise.

 

[Iron Woode]

Unfortunately for many it isn't obvious or are fully engaged in willful ignorance..too many people with auto-immune conditions participate in their own demise.

I don't deny that. I have personally seen it.

PS: I am a type 2 diabetic

 

[quikah]

This review outlines a hypothesis that A1 one of the common variants of beta-casein, a major protein in cows milk could facilitate the immunological processes that lead to type I diabetes (DM-I). It was subsequently suggested that A1 beta-casein may also be a risk factor for coronary heart disease (CHD), based on between-country correlations of CHD mortality with estimated national consumption of A1 beta-casein in a selected number of developed countries. A company, A2 Corporation was set up in New Zealand in the late 1990s to test cows and market milk in several countries with only the A2 variant of beta-casein, which appeared not to have the disadvantages of A1 beta-casein. https://pubmed.ncbi.nlm.nih.gov/15867940/

???

The second part of this review is a critique of the A1/A2 hypothesis. For both DM-I and CHD, the between-country correlation method is shown to be unreliable and negated by recalculation with more countries and by prospective studies in individuals. The animal experiments with diabetes-prone rodents that supported the hypothesis about diabetes were not confirmed by larger, better standardised multicentre experiments. The single animal experiment supporting an A1 beta-casein and CHD link was small, short, in an unsuitable animal model and had other design weaknesses. The A1/A2 milk hypothesis was ingenious. If the scientific evidence had worked out it would have required huge adjustments in the world's dairy industries. This review concludes, however, that there is no convincing or even probable evidence that the A1 beta-casein of cow milk has any adverse effect in humans. This review has been independent of examination of evidence related to A1 and A2 milk by the Australian and New Zealand food standard and food safety authorities, which have not published the evidence they have examined and the analysis of it. They stated in 2003 that no relationship has been established between A1 or A2 milk and diabetes, CHD or other diseases.

 

[Torn Mind]

If anyone ever tries to tell you dairy is a healthy food, you can ignore almost whatever they say after that. Childhood dairy intake has been shown to increase the risk of osteoporosis and all sorts of other not-so-good things, and they keep finding more.

Osteoporosis is caused by vitamin K2 deficiency. Fermentation will provide the K2, because via animal derivation or plant. Thus, a cheese product will be more effective than mere milk.

 

[mike8675309]

Osteoporosis is caused by vitamin K2 deficiency. Fermentation will provide the K2, because via animal derivation or plant. Thus, a cheese product will be more effective than mere milk.

The Purported Benefits of Vitamin K2: Should You Take Supplements? | NutritionFacts.org

Our body can make vitamin K2 from the K1 in green leafy vegetables.

nutritionfacts.org

There is no good evidence that vitamin K has bone, brain, or heart benefits beyond its blood-clotting function. And, even if such evidence arose, we can get all of the vitamin K we need from greens, since there’s no requirement specifically for vitamin K2. Further, if some evidence did arise that there was some unique benefit from K2, our microbiome makes K2 from the K1 in greens. What’s more, even if we had a problem with our microbiome, our own cells can make K1 from K2, just like other animals do. So, the bottom line is: Eat your greens.

 

[Torn Mind]

The Purported Benefits of Vitamin K2: Should You Take Supplements? | NutritionFacts.org

Our body can make vitamin K2 from the K1 in green leafy vegetables.

nutritionfacts.org

There is no good evidence that vitamin K has bone, brain, or heart benefits beyond its blood-clotting function. And, even if such evidence arose, we can get all of the vitamin K we need from greens, since there’s no requirement specifically for vitamin K2. Further, if some evidence did arise that there was some unique benefit from K2, our microbiome makes K2 from the K1 in greens. What’s more, even if we had a problem with our microbiome, our own cells can make K1 from K2, just like other animals do. So, the bottom line is: Eat your greens.

That's exploiting procedural presumption. That the evidence is not in, therefore it is conclusive proof that there is no effect is how this error in reasoning operates. If the reason that there is no evidence is because people didn't bother until 2007 or so(the Activator X that Weston Price could identify but was along with A and D, key in stopping caries, is indeed the very same K2), then there is immdiate bar from people experimenting with consuming K2 to improve their dental and bone condition. Because falling down and breaking a bone is a very real ender of the elderly, no matter how trivial as it sounds.

However, given that K2 activates two key bone enzymes, the more prudent approach is to eat in a manner that activates those precise enzymes until the evidence actually comes forward.

In the past, vitamin C preventing scurvy was not proven and validated in irrefutable science until the 20th century. But the British were already utilizing it based on "anecdote" 100 years earlier. Whereas, the Americans chose to go skeptical. Hindsight shows the British were not crazy for the 100 years the evidence was not 100% undisputable.

Veganism is but a mere category. One that alone, does not draw an inference beyond certain particular facts about the cells that make up the food(usually chlorophyll and cell walls). Fermentation is something that does not discriminate between animal or plant but is often key in manufacturing K2, i.e (natto).

Gregor is a sophist, and veganism is merely superior to the standard American diet, not an optimal diet.

The biological responses of vitamin K2: A comprehensive review

Vitamin K1 (VitK1) and Vitamin K2 (VitK2), two important naturally occurring micronutrients in the VitK family, found, respectively, in green leafy plants and algae (VitK1) and animal and fermented foods (VitK2). The present review explores the multiple ...

www.ncbi.nlm.nih.gov

 

[Torn Mind]

The retracted study by Kawai focused on multiple attempts at reducing osteoporosis. Even assuming that fraud was not there, K only had a "modest effect".

Kawai, even with the fraud, did not distinguish from K1 and K2. Just K. Gregor does technically only say "K", but leaves it to the usual stupid lay reader to mis-infer K means K2. He also leaves it to the listener or reader to mis-infer this statement applies to the entire body of studies, not the specific group of studies by a particular bunch of Japanese people. Not only does he leave it to the lay individual, they buy up his sophistry like blind sheep, as shown in the Youtube comments.

The actual "reasonable inference" from this fraudulent study alone is that neither form does anything and thus is not a reason to eat either greens or non-vegan foods containing either K vitamins.

Gregor's evidential foundation-building here is poor, and it's likely rampant throughout his work.

This how to distinguish between advocacy at all costs, which more similar to a lawyer uttering a statement, compared to a objective assessment. Gregor has also not objected to his bias and preferences, that animals need to be "saved", facts be damned.

If this is just start of Gregor's point-making, the others are probably just as sophist as this.

 

[Shmee]

I like beer and milk shakes.

 

[mike8675309]

I will make this very clear:

Type 1 diabetes is not caused by diet. It is an auto-immune disease.

Actually, there is some early evidence that environmental factors may play a larger role in causing Type 1 diabetes. One proposed path is dairy in childhood can contain mycobacterium avium paratuberculosis (causes Johne’s disease in ruminants including cows) , particularly in raw milk and raw milk products. But its DNA has been found in pasteurized dairy as well. MAP can trigger an immune response in the body and guess what else looks like MAP in the human body? Pancreatic beta cells responsible for insulin generation do.

...
then there is immdiate bar from people experimenting with consuming K2 to improve their dental and bone condition.
...

However, given that K2 activates two key bone enzymes, the more prudent approach is to eat in a manner that activates those precise enzymes until the evidence actually comes forward.
...

Torn, there is no current evidence of Vitamin K deficiencies in Americans. Americans should focus more on Vitamin D.
Nearly all elderly osteoporosis is related to the reduced nutrition that the elderly have because they just don't eat enough. They tend to eat less of a variety of food, and they eat less of it.

I found this to be a good source of some of the latest on Vitamin K.

 

[Torn Mind]

Actually, there is some early evidence that environmental factors may play a larger role in causing Type 1 diabetes. One proposed path is dairy in childhood can contain mycobacterium avium paratuberculosis (causes Johne’s disease in ruminants including cows) , particularly in raw milk and raw milk products. But its DNA has been found in pasteurized dairy as well. MAP can trigger an immune response in the body and guess what else looks like MAP in the human body? Pancreatic beta cells responsible for insulin generation do.




Torn, there is no current evidence of Vitamin K deficiencies in Americans. Americans should focus more on Vitamin D.
Nearly all elderly osteoporosis is related to the reduced nutrition that the elderly have because they just don't eat enough. They tend to eat less of a variety of food, and they eat less of it.

I found this to be a good source of some of the latest on Vitamin K.

No current evidence. Two ways that can be interpret, not one. They looked and couldn't find. Or, they didn't bother to look. Number 2 is the more likely scenario. The fact that it was even involved in bone was not known or simply not bothered with for decades.

And that video supports the importance of K2. Natto has the bacteria ferment the soybeans into a much more copious source of K2 than humans' innate conversion mechanism.

Obese individuals might eat plenty of K2, but it's stored in their fat cells and not used. Constant intake of a sugar or glucose assures a inhibition of releasing fat and vitamins stored attached to the fat.

 

[mike8675309]

No current evidence. Two ways that can be interpret, not one. They looked and couldn't find. Or, they didn't bother to look. Number 2 is the more likely scenario. The fact that it was even involved in bone was not known or simply not bothered with for decades.

And that video supports the importance of K2. Natto has the bacteria ferment the soybeans into a much more copious source of K2 than humans' innate conversion mechanism.

Obese individuals might eat plenty of K2, but it's stored in their fat cells and not used. Constant intake of a sugar or glucose assures a inhibition of releasing fat and vitamins stored attached to the fat.

Here is a link to one of the studies. Generally it seems what was done at that time was they knew environmental concerns impact type 1 diabetes. So they looked at possible environmental items. Diet being a big one, and dairy being something given to lots of children early, they looked at specific things in dairy that could cause problems.
So they figured out that thing that causes problems ,mycobacterium avium paratuberculosis, can survive in the milk from the cows. It can make it through pasteurization.

What they haven't figured out yet, and called out in the study is validated what happens in the human gut and the process that creates that immune response.

Mycobacterium avium subsp. paratuberculosis as a trigger of type-1 diabetes: destination Sardinia, or beyond?

Type 1 diabetes mellitus (T1DM) is a multifactorial autoimmune disease in which the insulin producing β cell population is destroyed by the infiltrated T lymphocytes. Even though the exact cause of T1DM is yet to be ascertained, varying degree ...

www.ncbi.nlm.nih.gov

Though MAP is identified as a trigger for T1DM, the underlying mechanism of MAP induced β-cell destruction is still an unsolved puzzle. As no easy animal model is available, development of an in vitro or an in vivo system will be of importance for deciphering the immunological network that is triggered in MAP pathogenesis, and that can be exploited for developing the functional evidence to link MAP to T1DM. It is also essential to understand the mechanisms by which mycobacteria such as MAP are acting as triggers in different autoimmune diseases and T1DM in particular. There is an urgent need to test a large number of geographically distinct patient populations with clinical T1DM in the same way as Sardinian patients have been tested for MAP. Also, it will be essential to develop high throughput genetic screens to identify single nucleotide polymorphisms that are associated with autoimmune diseases and those related to persistence of intracellular pathogens and a compensatory upregulation of proinflammatory cytokines. While it is important to identify other mycobacterial antigens that trigger host cell signaling cascades, it is certainly possible to scale up diagnostic screening tests based on existing antigens so that population level testing becomes practicable.

For decades, the population of Sardinia has been the subject of several human genetic analysis experiments. Population geneticists have revealed highly complex genetic relationships among Sardinians and other European populations. Peculiar gene pool characteristics of the Sardinians might have evolved over time as a function of strict isolation and consequent endogamy, consanguinity and the burden of historical scourges such as Malaria. High resolution, population based analyses are required to ascertain or negate any role of the unique Sardinian haplotypes and the high incidence of the autoimmune diseases.

Non-specific immune regulators such as Mycobacterium indicus pranii (MIP) [50] have been shown to play significant roles as immuno-therapeutic/prophylactic for leprosy, tuberculosis, leishmaniasis, psoriasis, bladder cancer and ano-genital warts [reviewed elsewhere - [51,52]]. It appears that non-specific immune stimulation could be the basic mechanism underlying the clearance of the lesions in all the above diseases when MIP was used. By analogy, MIP could also be used as a potential therapeutic/prophylactic agent for the autoimmune diseases rampant in Sardinia and beyond. It is essential therefore to test this organism in a setting such as Sardinia [53] as it has already worked wonderfully in a high burden country such as India which is crippled with tuberculosis, HIV, and diabetes. Given this, it will be tempting to propose experimental administration of MIP to susceptible populations and evaluate if it retards early onset of T1DM. Finally, the roles of intestinal microbiota and probiotic organisms should be explored at the interface of gut permeability and mucosal immunity [54] and the regulations thereof. Advancements in metagenomics of the gut microbiota and the consequent metabolomics and systems biology projects would be able to unravel the complex interactions underlying the alternative microbial mechanisms of T1DM apart from chronic MAP infection.