The Role of Meat and Dairy in Triggering Type 1 Diabetes

Type 1 diabetes “arises following the autoimmune destruction of the insulin-producing pancreatic β [beta] cells…[and] is most often diagnosed in children and adolescents, usually presenting with a classic trio of symptoms” as their blood sugars spike: excessive thirst, hunger, and urination. They need to go on insulin for the rest of their lives, since their own immune systems attacked and destroyed their ability to produce it. What would cause our body to do such a thing? I examine this in my video, Does Paratuberculosis in Milk Trigger Type 1 Diabetes?

Whatever it is, it has been on the rise around the world, starting after World War 2. “Understanding why and how this produced the current pandemic of childhood diabetes would be an important step toward reversing it.” A plausible guess is “molecular mimicry, whereby a foreign antigen (bacterial or viral) provokes an immune response, which cross-reacts” with a similar-looking protein on our pancreas such that when we attack the bug, our own organ gets caught in the cross-fire. Given this, what pancreatic proteins are type 1 diabetics self-attacking? In the 1980s, a protein was identified that we came to realize in the 1990s looked an awful lot like a certain mycobacterial protein. Mycobacteria are a family of bacteria that cause diseases like tuberculosis and leprosy, and, in one study, all newly diagnosed type 1 diabetic children were found to have immune responses to this mycobacterial protein. This didn’t make any sense as incidence of type 1 diabetes has been going up in the industrialized world, whereas TB and leprosy rates have gone down. However, there is one mycobacterial infection in farm animals that has shot up with the industrialization and globalization of animal agriculture: paratuberculosis (paraTB), which causes Johne’s disease in animals. Paratuberculosis is now recognized as a global problem for the livestock industry.

Weren’t there a dozen or so studies suggesting that “cow’s milk exposure may be an important determinant of subsequent type 1 diabetes” in childhood? Indeed. After putting two and two together, an idea was put forward in 2006: Could mycobacterium paratuberculosis from cattle be a trigger for type 1 diabetes? The idea was compelling enough for researchers put it to the test.

They attempted to test the association of Mycobacterium avium paratuberculosis (MAP), the full name for the bug, with type 1 diabetes by testing diabetics for the presence of the bacteria in their blood. Lo and behold, most of the diabetic patients tested positive for the bug, compared to only a minority of the healthy control subjects. This evidence of MAP bacteria in the blood of patients with type 1 diabetes “might provide an important foundation in establishing an infectious etiology,” or cause, for type 1 diabetes. “These results also might possibly have implications for countries that have the greatest livestock populations and high incidence of MAP concurrent with the highest numbers of patients with” diabetes, like the United States.

Johne’s is the name of the disease when farm animals get infected by MAP. The reason diabetes researchers chose to look at Sardinia, an island off the coast of Italy, is because paratuberculosis is present in more than 50 percent of Sardinian herds. Surpassing that, though, is the U.S. dairy herd. According to a recent national survey, 68 percent of the U.S. dairy herd are infected with MAP, especially those cattle at big, industrial dairies, as you can see at 3:33 in my video. Ninety-five percent of operations with more than 500 cows came up positive. It’s estimated the disease costs the U.S. industry more than a billion dollars a year.

How do people become exposed? “The most important routes of access of MAP to the [human] food chain appear to be contaminated milk, milk products and meat” from infected cattle, sheep, and goats. MAP or MAP DNA has been detected in raw milk, pasteurized milk, infant formula, cheese, ice cream, muscle and organ tissues, and retail meat. We know paraTB bacteria survive pasteurization because Wisconsin researchers bought hundreds of pints of retail milk off store shelves from three of the top U.S. milk-producing states and tested for the presence of viable, meaning living, MAP bacteria. They found that 2.8 percent of the retail milk tested came back positive for live paraTB bacteria, with most brands yielding at least one positive sample. If paraTB does end up being a diabetes trigger, then “these findings indicate that retail milk [in the United States] would need to be considered as a transmission vector.” Why hasn’t the public heard about this research? Perhaps because the industry is not too keen on sharing it. Indeed, according to an article in the Journal of Dairy Science: “Fear of consumer reaction…can impede rational, open discussion of scientific studies.”

Not only is MAP a serious problem for the global livestock industry, but it also may trigger type 1 diabetes, given that paraTB bacteria have been found in the bloodstream of the majority of type 1 diabetics tested who presumably are exposed through the retail milk supply as the bacteria can survive pasteurization. But what about the meat supply? MAP has been found in beef, pork, and chicken. It’s an intestinal bug, and unfortunately, “[f]aecal contamination of the carcass in the abattoir [slaughter plant] is unavoidable…” Then, unless the meat is cooked well-done, it could harbor living MAP.

In terms of meat, “ground beef represents the greatest potential risk for harboring MAP…[as] a significant proportion originates from culled dairy cattle,” who may be culled because they have paratuberculosis. These animals may go straight into the human food chain. There also exists greater prevalence of fecal contamination and lymph nodes in ground meat, and the grinding can force the bacteria deep inside the ground beef burger. As such, “given the weight of evidence and the severity and magnitude of potential human health problems, the precautionary principle suggests that it is time to take actions to limit…human exposure to MAP.” At the very least, we should stop funneling animals known to be infected into the human food supply.

We know that milk exposure is associated with type 1 diabetes, but what about meat? As I discuss in my video Meat Consumption and the Development of Types 1 Diabetes, researchers attempted to tease out the nutritional factors that could help account for the 350-fold variation in type 1 diabetes rates around the world. Why do some parts of the world have rates hundreds of times higher than others? Yes, the more dairy populations ate, the higher their rates of childhood type 1 diabetes, but the same was found for meat, as you can see at 2:07 in my video. This gave “credibility to the speculation that the increasing dietary supply of animal protein after World War II may have contributed to the reported increasing incidence of type 1 diabetes…” Additionally, there was a negative correlation—that is, a protective correlation that you can see at 2:26 in my video—between the intake of grains and type 1 diabetes, which “may fit within the more general context of a lower prevalence of chronic diseases” among those eating more plant-based diets.

What’s more, the increase in meat consumption over time appeared to parallel the increasing incidence of type 1 diabetes. Now, we always need to be cautious about the interpretation of country-by-country comparisons. Just because a country eats a particular way doesn’t mean the individuals who get the disease ate that way. For example, a similar study looking specifically at the diets of children and adolescents between different countries “support[ed] previous research about the importance of cow’s milk and [other] animal products” in causing type 1 diabetes. But, the researchers also found that in countries where they tended to eat the most sugar, kids tended to have lower rates of the disease, as you can see at 3:18 in my video. This finding didn’t reach statistical significance since there were so few countries examined in the study, but, even if it had and even if there were other studies to back it up, there are countless factors that could be going on. Maybe in countries where people ate the least sugar, they also ate the most high fructose corn syrup or something. That’s why you always need to put it to the test. When the diets of people who actually got the disease were analyzed, increased risk of type 1 diabetes was associated with milk, sugar, bread, soda, eggs, and meat consumption.

In Sardinia, where the original link was made between paraTB and type 1 diabetes, a highly “statistically significant dose-response relationship” was found, meaning more meat meant more risk, especially during the first two years of children’s lives. So, “[h]igh meat consumption seems to be an important early in life cofactor for type 1 diabetes development,” although we needed more data.

The latest such study, which followed thousands of mother-child pairs, found that mothers eating meat during breastfeeding was associated with an increased risk of both preclinical and full-blown, clinical type 1 diabetes by the time their children reached age eight. The researchers thought it might be the glycotoxins, the AGEs found in cooked meat, which can be transferred from mother to child through breastfeeding, but they have learned that paratuberculosis bacteria can also be transferred through human breast milk. These bacteria have even been grown from the breast milk of women with Crohn’s disease, another autoimmune disease linked to paraTB bacteria exposure.


For a deeper discussion of other possibilities as to why cow’s milk consumption is linked to this autoimmune destruction of insulin production, see Does Casein in Milk Trigger Type 1 Diabetes? and Does Bovine Insulin in Milk Trigger Type 1 Diabetes?.

If we don’t drink milk, though, what about our bone health? See my videos Long-Term Vegan Bone Health and Is Milk Good for Our Bones?.

The vast majority of cases of diabetes in the United States are type 2, though. Ironically, meat may also play a role there. See my videos Why Is Meat a Risk Factor for Diabetes? and How May Plants Protect Against Diabetes? for more information.

For more on the links between milk and diabetes, see my videos Does Casein in Milk Trigger Type 1 Diabetes? and Does Bovine Insulin in Milk Trigger Diabetes?. What about treating and preventing diabetes through diet? Check out How Not to Die from Diabetes and How to Prevent Prediabetes from Turning Into Diabetes.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

How Not to Die from Kidney Disease

Kidney failure may be both prevented and treated with a plant-based diet, and it’s no wonder: Kidneys are highly vascular organs, packed with blood vessels. Harvard researchers found three significant dietary risk factors for declining kidney function: “animal protein, animal fat, and cholesterol.” Animal fat can alter the actual structure of our kidneys. In my video How Not to Die from Kidney Disease, you can see plugs of fat literally clogging up the works in autopsied human kidneys from a study published in The American Journal of Pathology.

Animal protein can have a “profound effect” on normal kidney function, inducing “hyperfiltration,” increasing the workload of the kidney. Not plant protein, though. After eating a meal of tuna fish, the increased pressure on the kidneys goes up within only a few hours. We aren’t talking about adverse effects decades down the road, but literally within hours of it going into our mouths. What happens if, instead of having a tuna salad sandwich, you had a tofu salad sandwich with the exact same amount of protein? No effect on your kidneys. Our kidneys have no problem dealing with plant protein is no problem.

Why does animal protein cause the overload reaction, but plant protein doesn’t? It appears to be due to the inflammation triggered by the consumption of animal products. Indeed, taking a powerful, anti-inflammatory drug along with that tuna fish sandwich can abolish the hyperfiltration, protein-leakage response to meat ingestion.

There’s also the acid load. Animal foods, such as meat, eggs, and dairy, induce the formation of acid within the kidneys, which may lead to “tubular toxicity,” damage to the tiny, delicate, urine-making tubes in the kidney. Animal foods tend to be acid-forming—especially fish, which is the worst, followed by pork and poultry—whereas plant foods tend to be relatively neutral, or actually alkaline or base-forming to counteract the acid, especialy green leafy vegetables. So, “[t]he key to halting progression of CKD [chronic kidney disease] might be in the produce market, not in the pharmacy.”

It’s no wonder plant-based diets have been used to treat kidney disease for decades. In my video, you can see a remarkable graph that follows the protein leakage of subjects first on a conventional, low-sodium diet, which is what physicians would typically put someone with declining kidney function on, then switched to a supplemented vegan diet, back to the conventional diet, once more on the plant-based diet, and back and forth again. The chart is filled with zig-zags, showing kidney dysfunction was effectively turned on and off like a light switch, based on what was going into their mouths.


The first time someone visits NutritionFacts.org can be overwhelming. With videos on more than 2,000 health topics, where do you even begin? Imagine stumbling onto the site not knowing what to expect and the new video-of-the-day is about how a particular spice can be effective in treating a particular form of arthritis. It would be easy to miss the forest for the trees, which is precisely why I created a series of overview videos that are essentially taken straight from my live, hour-long 2016 presentation How Not to Die: Preventing, Arresting, and Reversing Our Top 15 Killers.

For the other videos in this overview series, see:

Inspired to learn more about the role diet may play in preventing and treating kidney disease? Check out these other popular videos on the topic:

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

How Can Animal Protein Intake Increase Childhood Obesity Risk?

If pregnant crickets are exposed to a predatory wolf spider, their babies will hatch, exhibiting increased antipredator behavior and, as a consequence, improved survival from wolf spider attack. The mother cricket appears to be able to forewarn her babies about the threat when they are still inside her, so they would be pre-adapted to their external environment. This even happens in plants. If you grow two genetically identical plants—one in the sun, one in the shade—the sun-grown plant will produce seeds that grow better in the sun, and the shaded plant will produce seeds that grow better in the shade—even though they’re genetically identical.

What’s happening is called epigenetics, external factors changing gene expression.

Vole pups born in the winter come out growing thicker coats. Vole mothers are able to communicate the season to their babies in utero and tell them to put a coat on even before they’re born. We’re no different. You know how some people have different temperature tolerances, resulting in “battles of the bedroom”? Do you turn the AC on or off? Open the windows? It’s not just genetics. Whether we’re born in the tropics or in a cold environment determines how many active sweat glands we have in our skin.

What does this have to do with diet? As I discuss in my video Animal Protein, Pregnancy, and Childhood Obesity, can what a pregnant woman eats—or doesn’t eat—permanently alter the biology of her children in terms of what genes are turned on or off throughout life?

What happened to the children born during the 1944 – 1945 Dutch famine imposed by the Nazis? They had higher rates of obesity 50 years later. The baby’s DNA gene expression was reprogrammed before birth to expect to be born into a world of famine and conserve calories at all cost. But when the war ended, this propensity to store fat became a disadvantage. What pregnant women eat and don’t eat doesn’t just help determine the birth weight of the child, but the future adult weight of the child.

For example, maternal protein intake during pregnancy may play a role in the obesity epidemic—but not just protein in general. “Protein from animal sources, primarily meat products, consumed during pregnancy may increase risk of overweight in offspring…” Originally, researchers thought it might be the IGF-1, a growth hormone boosted by animal product consumption, that may increase the production of fatty tissue, but weight gain was tied more to meat intake than dairy. Every daily portion of meat intake during the third trimester of pregnancy resulted in about an extra 1 percent of body fat mass in their children by their 16th birthday, potentially increasing their risk of becoming obese later in life, independent of how many calories they ate or how much they exercised.  But no such link was found with cow’s milk intake, which would presumably boost IGF-1 levels just as high.

Given that, perhaps instead of IGF-1, it’s the obesogens in meat, chemicals that stimulate the growth of fatty tissue. “[E]merging evidence demonstrates that environmental factors can predispose exposed individuals to gain weight, irrespective of diet and exercise.” After all, even our infants are fatter, and we can’t blame that on diet and exercise. Animals are fatter, too, and not just our pampered pets—even rats in laboratories and subways are bigger. “The likelihood of 24 animal populations from eight different species all showing a positive trend in weight over the past few decades by chance was estimated at about 1 in 10 million” so it appears something else is going on—something like obesogenic chemicals.

One such candidate is polycyclic aromatic hydrocarbons (PAHs), which are found in cigarette smoke, vehicle exhaust, and grilled meat. A nationwide study of thousands found that the more children were exposed to PAHs, the fatter they tended to be. The researchers could measure the level of these chemicals right out of their urine. Exposure can start in the womb. Indeed, prenatal exposure to these chemicals may cause increased fat mass gained during childhood and a higher risk of childhood obesity.

If these pollutants sound familiar, I’ve covered them before in relation to increasing breast cancer risk in the Long Island Breast Cancer Study Project. So, perhaps they aren’t just obesogens, but carcinogens, as well, which may help explain the 47 percent increase in breast cancer risk among older women in relation to a lifetime average of grilled and smoked foods.

If we look at one of the most common of these toxins, smokers get about half from food and half from cigarettes. For nonsmokers, however, 99 percent comes from diet. The highest levels of PAHs are found in meat, with pork apparently worse than beef. Even dark green leafies like kale can get contaminated by pollutants in the air, though, so don’t forage for dandelion greens next to the highway and make sure to wash your greens under running water.

These are fat-soluble pollutants, so they need lots of fat to be absorbed. It’s possible that even heavily contaminated plant-based sources may be safer, unless you pour lots of oil on your food, in which case the toxins would presumably become as readily absorbed as the toxins in meat.

The good news is they don’t build up in our body. As I show in my video, if we expose people to barbecued chicken, they get a big spike in these chemicals—up to a hundred-fold increase—but our body can get rid of them within about 20 hours. The problem, of course, is that people who eat these kinds of foods every day could be constantly exposing themselves, which may not only affect their health and their children’s health, but maybe even their grandchildren’s health.

Being pregnant during the Dutch famine of the mid-1940s didn’t just lead to an increase in diseases among their kids, but even apparently their grandkids. What a pregnant woman eats now may affect future generations. “The issue of generation-spanning effects of poor conditions during [pregnancy]…may shed light on the epidemic of diabetes, obesity and cardiovascular disease,” which is associated with the transition towards Western lifestyles.


Epigenetics is the science of altering the expression of our genes. No matter our family history, some genes can be effectively turned on and off by the lifestyle choices we make. See, for example:

For more on “obesogenic” chemicals, see:

I previously touched on PAHs in Meat Fumes: Dietary Secondhand Smoke.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations: