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  • Writer's picturePaul Magee Berry

Got Diabetes?

Currently 84 MILLION Americans have “prediabetes” and Dairy consumption is a contributing factor.

Today, there are over 30 million Americans living with diabetes. About 5% of cases are type 1 diabetes, and about 95% are type 2 diabetes. The CDC estimates that another 84 MILLION Americans currently have “prediabetes” as well, which means they are on track to develop the full disease (type 2) in 5 years or less. It means that today, one in every three Americans (33.8%) currently have diabetes or prediabetes [1].

And over the next decade, the total number of Americans with diabetes will DOUBLE [2].

Diabetes is currently the 7th highest killer of Americans, the #1 cause of adult blindness, kidney failure, and lower-limb amputations. Diabetes also increases the risk of heart disease and stroke by 65%. In the last 20 years, the number of adults diagnosed with diabetes has more than tripled– the epidemic of the disease is growing exponentially (see Fig. 1), and so are the costs.

Total annual costs for diabetes in America is already well over $300 billion per year. That number is predicted to double over the next decade, following the rising number of diabetes cases [3]. But the cost of diabetes could easily TRIPLE over the next decade unless price-fixing by BigPharma is reined in and regulated: wholesale prices for the most common insulins have alreadytripled over the past decade4.

Of course, insulin therapy is the “key” drug treatment for those with type 1 diabetes. Insulin is a naturally occurring hormone that “unlocks” the cells in our body to transport blood sugar (glucose) from the bloodstream into our cells. Our cells use the glucose for energy as needed and then store the rest. Normally, insulin is produced by our pancreas and released into the bloodstream whenever blood sugar levels rise, like after a meal. But for those with Type 1 diabetes, their pancreas is no longer able to produce the hormone. Without insulin, blood sugar can’t enter the cells; the cells’ energy reserves become depleted, and blood sugar level rises. Chronic levels of high blood sugar can cause serious health threats including a condition called diabetic ketoacidosis which could lead to loss of consciousness and, eventually, death.

Type 2 diabetes operates differently than type 1 diabetes. In type 2 diabetics, the pancreas can still produce insulin, but the body has built up a gradual resistance to it (insulin resistance). With insulin resistance, the cells have become clogged with too much fat and fatty toxins which inhibit the transport of blood sugar into the cells [5]. Over time, a high-fat diet– especially a diet high in saturated fats [6] will require more and more insulin production from the pancreas to manage blood sugar levels. Eventually, chronic insulin resistance in type 2 diabetics can surpass the insulin productivity of the pancreas and require insulin therapy.

Sidebar here on high-fat keto diets?

Some doctors and researchers consider type 1 diabetes (T1D) and type 2 diabetes (T2D) different diseases with different origins. Some consider T1D an autoimmune disease (see “autoimmunity” below), and T2D a metabolic disorder (how the body converts food to energy). Certainly, the independent (non-corporate funded) research reveals that both types of diabetes share important cofactors in their causation which provide clues to their prevention. Following is a summary of the best research available on T1D. We cover Type 2 diabetes in a separate article.

[Editor’s note: the following summary of research on type 1 diabetes is informed by Dr. Michael Greger’s two-volume, 3-part video series on type 1 and type 2 diabetes. Links to the full video series (total 6 videos about 6 mins each) for each type are provided in the Endnotes below.]*

In 1991, type 1 diabetes (T1D) was defined in the scientific literature as a disease in which the immune system attacks and destroys the insulin-producing cells of the pancreas7. When the immune system attacks the body in such a way, scientists refer to the phenomenon as “autoimmunity”. Autoimmunity is a “pathway” for the development of various common diseases, including T1D, celiac, lupus, multiple sclerosis and many others.

Over the past several decades, scientific research on T1D has primarily focused on three broad areas: how to treat T1D to relieve the effects of the disease, the causes of T1D, and its cure. This article focuses on the research re: causation, and more specifically, the research that asks, “what are the mechanisms that trigger T1D autoimmunity, and how can T1D autoimmunity be prevented in the first place?

Most scientists agree that the most plausible pathway for the development of T1D autoimmunity is that of “molecular mimicry” [8], where a foreign molecule enters the body and provokes an immune response; the immune system then releases certain proteins (called antibodies) to destroy the foreign molecules (called antigens), but those antibodies end up destroying certain of the body’s own cells as well. In the case of autoimmunity in T1D, the invading molecule is thought to “mimic” certain attributes of the pancreatic cells that normally produce our insulin. Over time, as insulin-producing cells are inadvertently destroyed by the body’s own antibodies, insulin production is destroyed, and the T1D patient will require insulin therapy for survival.

The various research into T1D autoimmunity has followed two main tracks: (I) genetic research on predisposition to T1D autoimmunity (i.e., which genes predispose us to T1D autoimmunity), and (II) research into the environmental factors (dietary, viral, bacterial, etc) that “trigger” the autoimmunity in those who are genetically predisposed. Following are brief summaries of the research on each.

Every human has the same general set of genes– about 21,000 in all– but each individual gene can have multiple variants, 100s of millions in total. And among all those variants, no single “diabetes gene” has yet been discovered that gets activated (or deactivated) to cause the disease. But scientists have now identified more than 40 genes that can influence an individual’s predisposition or susceptibility to T1D [9]. These include a group of genes that influence our immune response, and in which certain variants of these genes are present in up to 50% of T1D patients. Notably, followup research has shown that less than 10% of people born with these “high- susceptibility” genes ever develop T1D [10] (more on that in Section II below on Environmental Triggers).

As genetic research has progressed and the list of T1D susceptibility genes has grown– including new gene groups, large in quantity but small in effect– more and more researchers agree that T1D autommunity is most likely influenced by multiple genes and with limited predictability [11]. However, researchers have narrowed down the probable T1D antibodies (the proteins released by the immune system) that are responsible for attacking the body’s pancreatic cells (see “molecular mimicry” above). Scientists refer to these antibodies as “T1D autoantibodies”, and find further that the presence of two or more T1D autoantibodies in a person’s blood sample can substantially improve the predictability of whether they will eventually develop the disease [12].

The research has also narrowed down certain general characteristics of the probable T1D antigen(s). Antigens are the foreign molecules that enter the body and “trigger” the production of autoantibodies [13]. No single causal antigen has yet been confirmed for T1D, but researchers have determined that the presence of certain antigens in the bloodstream significantly improve predictability of T1D [14].

Research into family genetics has also informed T1D predictability. For example, in identical twins there’s about a 50% chance that if one gets the disease, the other may get it too. And the risk of T1D for siblings of diabetics is found to be 15-fold higher than the risk of T1D in the general population. But researchers have found that only 10% of new T1D patients have a family member with T1D [15]. So family genetics can only account for a fraction of new T1D cases and even then with only limited predictability.

Similarly, research into population genetics has found that some countries have very low rates of T1D compared to other countries. For example, the incidence of T1D in America is 18 times higher than in Japan. In fact, incidence rates can vary from country to country by more than 350 fold [16]. Some countries have rates of diabetes that are hundreds of times higher than others. But again, population genetics concludes that genetics alone has limited predictability; e.g., when children migrate from low- to high- incidence regions, they tend to acquire the risk of their new home [17].

To-date, the results of genetic research into causation of T1D suggest that while genes seem to play an important role in the progression of the disease, “our genes are not our fate”, and “the most crucial determinant in the development of T1D is environment (i.e., the external factors (antigens) that trigger T1D autoimmunity). [18] [19]”

A survey of the independent (non-corporate-funded) research on environmental factors for T1D reveals that scientists have zeroed in on a set of primary antigens that alone or in combination with secondary factors trigger the release of T1D autoantibodies, and thus represent primary causation for T1D. Following is a brief sampling of the relevant research on each:

One of the autoantibodies that gets triggered in T1D is an autoantibody that attacks insulin. It seems counter-intuitive that the body’s own immune system would manufacture an antibody to attack a molecule that it produces for its own survival. But indeed, researchers found that one of the primary antibodies present in the blood of test subjects who later develop T1D is an insulin autoantibody (IAA) [20] [21].

In follow-up research, scientists found the plausible explanation in a study of children who were fed infant formula to supplement or replace their mother’s breast milk. Infant formula is made from cow’s milk, and cow’s milk contains cow’s insulin which closely resembles the structure of our own insulin. Researchers conducted a randomized double blind trial, comparing blood samples from infants who were fed two different types of cow’s milk formula– the regular infant formula recorded in the previous study, and a new modified infant formula in which the cow insulin was removed. And the results confirmed that, indeed “[the cow insulin] in cow’s milk formula induces primary autoimmunity to insulin in infants who are at genetic risk for type 1 diabetes [22]”

In a more recent study published in the prestigious Journal Nature, scientists combined epidemiological, laboratory, and theoretical research to conclude that “a complex interplay between dietary triggers, permissive gut factors, and potentially other influencing factors underpins disease progression [in T1D]. The results of the study revealed comprehensive evidence that the protein in cows’ milk is the dominant causal trigger of type 1 diabetes. [23]

The researchers also acknowledged that cows’ insulin and wheat gluten [24] can be primary dietary triggers as well, but conclude that cows’ milk protein is the dominant dietary trigger. They also identify “other influencing factors”, including exposure to milk protein through breastfeeding by mothers who consume dairy-based foods [25], vitamin D deficiency, and permissive gut (intestinal permeability).

The research on cows’ insulin was explored in the preceding section above, which concludes that, “the insulin in cow’s milk formula induces primary autoimmunity to insulin in infants at genetic risk for type 1 diabetes [26]” And the evidence for wheat gluten [27] and Vitamin D (deficiency) as additional dietary triggers in the present study is strong, especially for wheat gluten, but the latter are beyond the scope of this article.

In exploring cows’ milk protein (called casein) as a dietary trigger for T1D, the researchers studied autoimmune responses to the two main types of cows’ milk protein: A1 casein and A2 casein. About 95% of U.S. dairy cows and most of the global dairy cows produce milk with A1 casein [28]. Scientists found that when milk is digested, the A1 casein breaks down into “casomorphin”, a protein that has opioid properties which can alter immune function and increase susceptibility to certain infections that can trigger T1D autoimmunity.[29] The A2 casein does not produce this casomorphin.

Foundational to these findings is the researchers’ hypothesis that “permissive gut factors” (intestinal permeability) is a precondition for establishing T1D autoimmunity. Other studies have found that supplementing breast milk with infant formula can compromise intestinal permeability and have long-term consequences on immune health [30]. When intestinal permeability is compromised, undigested food proteins, and bacteria and other toxins can “leak” through the infant’s intestines, enter the bloodstream, and cause an autoimmune response, including the production of T1D autoantibodies to cows’ insulin, A1 casein, and casomorphin as explained above.

In children who are predisposed to diabetes, the presence of two or more such autoantibodies is associated with a risk of progression to clinical diabetes of about 60% to 80% [31]. Indeed, most scientists today agree that “individuals genetically at risk of T1D with at least two T1D autoantibodies are at such a high risk of progression to clinical disease that they can be regarded as having type 1 diabetes” [32].

Compounding the evidence on A1 casein, the researchers also cited a population study published in the New Zealand Medical Journalthat examined food consumption data from 19 different ‘health care affluent’ countries. The study focused on correlations between food consumption and the rates of type 1 diabetes, and researchers found “extremely high” correlations between the consumption of A1 casein and the incidence of T1D, but not for A2 casein [33]. In fact, a total of 15 different food variables were studied including cows’ milk with both A1 and A2 casein, and the cows’ milk with A1 casein scored higher for T1D incidence than all the other foods investigated.

T1D incidence was highest in Finland and Sweden (the two countries with the highest per capita A1 casein consumption per capita), and lowest in Venezuela and Japan (the two countries with the lowest per capita A1 casein consumption [34].

Combining the evidence of this population study with the evidence on A1 casein autoimmunity in the molecular research of cited above, the researchers observe that “no plausible explanation has emerged that would invalidate this ‘extremely high’ evidential relationship between A1 casein and T1D incidence.” The authors conclude that, “on the balance of probabilities..” A1 casein milk is the dominant trigger for T1D, with permissive gut factors as a primary co-factor influenced by timing, magnitude and/or duration of exposure.” And that “within this framework, the removal of [A1 casein milk] could profoundly affect type 1 diabetes incidence.”

Genetic research into type 1 diabetes (T1D) has identified certain “high susceptibility” genes that predispose people to developing T1D. However, even the “highest-susceptibility” genes that have been identified provide only limited predictability. Research into hereditary genetics has produced similar results. For example, in identical twins, there is only about a 50% chance that a diabetic’s twin will develop the disease. And only about 10% of newly diagnosed diabetics have a family member with the disease.

Molecular research into the mechanisms of T1D progression has been productive. Certain antibodies involved in T1D autoimmunity have been identified, as well as specific dietary antigens that trigger those autoantibodies. Confirmation of those antigens has been further reinforced by randomized double-blind studies. And the certainty of those T1D antigens has been triply confirmed by population studies that tracks their rates of consumption against T1D incidence rates.

There is such significant, compounding evidence that scientists now conclude with “extremely high” confidence that “a complex interplay between dietary triggers, permissive gut factors, and potentially other influencing factors underpins the progression of type 1 diabetes.” And that “the protein in cows’ milk is the dominant causal trigger of type 1 diabetes. [35]

In seems that much of the key data for T1D prevention have been available for the past few decades, and scientists are just putting all the evidence together now. But it does beg the question: why haven’t the major funders of diabetes research proclaimed these latest observations on A1 casein? Even as the researchers of the A1 casein study above proclaim, “the removal of [A1 casein milk] could profoundly affect type 1 diabetes incidence.“?

The “A1 casein..” study was published in 2017 in the prestigious scientific journal Nature, which is ranked as the world’s most cited scientific journal and one of the world’s top academic journals [36]. But there was no mention of the study by the top NGOs that fund diabetes research, The American Diabetic Association and Diabetes UK.

However, within just a few months of the study’s publication, Diabetes UK released an article (now retracted) claiming, “A new study shows no evidence that cow's milk is a causal factor in type 1 diabetes.” Really? The study they cited was a very narrow comparison of intact casein versus processed (hydrolyzed) casein in infant formula. . Certainly BigDairy was hoping their hydrolyzed protein would trigger less type 1 diabetes, but the research proved “no change” [38]. I.e., whether the cows’ protein in infant formula is intact casein or hydrolyzed casein, the cows’ casein in infant formula is still a trigger for T1D*. That would have been a truthful claim that would inform pregnant and nursing mothers who are concerned about diabetes. Why the deceptive article from Diabetes UK?

Diabetes UK is considered the “foremost UK diabetes charity”, but their deceptive article above is not the organization’s only controversy, including being exposed for “blood money” deals with industry. But the reigning champion of corporate donations is the American Diabetes Association.

The Top Tier Donors of the American Diabetes Association (at $1 million or more each) is a Who’s Who list of BigPharma [39] including Eli Lilly, Novo Nordisk, and Sanofi- the three drug manufacturers of insulin in the US– as well as Abbott, AstraZeneca, BD Medical-Diabetes Care, Boehringer Ingelheim Pharmaceuticals, Dexcom,, Janssen Pharmaceuticals, and Merck.

And it seems the American Diabetes Association completely ignored the “A1 casein..” study as well. But again, within just months of that study, the American Diabetes Association promoted a different study, though similarly titled, “Scientist Identifies Possible Trigger for Type 1 Diabetes” [40] Their announcement was even parroted by CBS news [41]. But the study had nothing to do with an external “trigger” for type 1 diabetes. Instead, their study described “a modification of the body’s insulin that acts as an antigen”, but the study did not investigate what external factor triggers that modification, as did the “A1 casein..” study.

It would take a spectacular feat of naivety to dismiss these two examples as coincidental oversight. Especially considering that the American Diabetes Association and Diabetes UK carry $10s of millions in annual staff salaries funded by $10 of millions in annual donations from BigPharma corporations that make $100s of billions in revenues from diabetes suffers off drug treatments; considering further that wholesale prices for the most common insulins have already tripled over the past decade [42]; and that BigPharma revenues on T1D treatments are expected to double again over the next decade [43]… The #1 priority for drug corporations is profit. According to a Goldman Sachs report on Biotech Research, curing patients is not a sustainable business model.

If BigPharma and its surrogate NGOs– and especially BigDairy– purposely ignore such breakthrough research as the “A1 casein” study and the myriad other research over the past few decades that link dairy as a trigger for T1D, it’s not just a systemic industry coverup. It’s a cruel and deadly consumer fraud much like BigTobacco and its surrogate researchers perpetrated on cigarette smokers who suffered lung cancer. And it deserves official congressional inquiry, just as BigTobacco did.

Of course, that historic inquiry and settlement with BigTobacco didn’t stop BigTobacco’s profiteering– it just went global. And as type 1 diabetes, obesity, and heart disease spread globally at “alarming rates” [44], It’s why independent (non-corporate funded) scientists formed the The Global Syndemic to reduce the influence of large commercial interests in the public policy development process; to enable global governments to implement policies in the public interest to benefit the health of current and future generations…”

Given the preponderance of scientific evidence that links cows’ milk and dairy-based foods to chronic diseases such as type 1 diabetes, heart disease, obesity, Alzheimer’s disease, various cancers and other debilitating diseases, the U.S. Dietary Guidelines (DGA) for Americans should not be promoting milk nor any dairy-based foods. The DGA is funded by our tax dollars, and our tax dollars should not be encouraging a disease-for-profit food system built on the toxic proteins and saturated fats of dairy- based foods. For more information please see our campaign to #DefundBigMeat.

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  2. Calculate Your Food Carbon Footprint, and

  3. Sign the Petition to #DefundBigMeat

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*Two-Volume Video Series on Type 1 and Type 2 Diabetes

By Dr. Michael Greger of

Volume I — Type 1 Diabetes Overview

By Dr. Michael Greger of

Episode 1 – “Does Casein in Milk Exposure Trigger Type 1 Diabetes?”

Episode 2 – “Does Bovine Insulin in Milk Trigger Type 1 Diabetes?”

Episode 3 – “Does Paratuberculosis in Milk Trigger Type 1 Diabetes?”

Volume II — Type 2 Diabetes Overview

By Dr. Michael Greger of

Episode 1 – “What Causes Insulin Resistance?”

Episode 2 – “The Spillover Effect Links Obesity to Diabetes”

Episode 3 – “Lipotoxicity: How Saturated Fat Raises Blood Sugar”

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  2. Centers for Disease Control & Prevention, “National Diabetes Statistics Report,”, 2017,

  3. William R. Rowley, MD; Clement Bezold, PhD; Yasemin Arikan, BA; Erin Byrne, MPH; and Shannon Krohe, “Diabetes 2030: Insights from Yesterday, Today, and Future Trends,” US National Library of Medicine, National Institutes of Health, February 1, 2017,

  4. Elisabeth Rosenthal, MD, “When High Prices Mean Needless Death,” JAMA Internal Medicine, JAMA Network, January 2019,

  5. M Krssak; Petersen K Falk; A Dresner; L DiPietro, SM Vogel; DL Rothman; M Roden; GI Shulman, “Intramyocellular lipid concentrations are correlated with insulin sensitivity in humans: a 1H NMR spectroscopy study,” US National Library of Medicine, National Institutes of Health, January 1999,

  6. T Maric; B Woodside; GN Luheshi, “The effects of dietary saturated fat on basal hypothalamic neuroinflammation in rats,” US National Library of Medicine, National Institutes of Health, February, 2014,

  7. D. Andreani; U. Di Mario; P. Pozzilli, “Prediction, prevention, and early intervention in insulin‐dependent diabetes,” Wiley Online Library, March 1991,

  8. Ken T Coppieters; Anna Wiberg; Matthias G Von Herrath, “Viral infections and molecular mimicry in type 1 diabetes,” US National Library of Medicine, National Institutes of Health, October 11, 2012,