Milk Consumption Is Linked to Type 1 Diabetes

Type 1 diabetes, which typically strikes children and young adults, is an autoimmune disease in which our own immune system attacks and destroys the insulin-producing cells of our pancreas. Untreated it’s deadly, but even with well-managed insulin replacement, it may shorten life expectancy by a decade. “Families are devastated when a child receives a diagnosis of type 1 diabetes…Thus, one of modern medicine’s ‘holy grails’” is to understand what causes the body to attack itself, in the hopes that we can cure or prevent the disease. Genetic susceptibility plays an important role, but the “concordance for type 1 diabetes is only about 50% among identical twins.” So, even if someone with our exact same DNA gets the disease, there’s only about a 50 percent chance we will get it, too—meaning there must be external factors as well.

Some countries have low rates of incidence, and others have high rates. Japan, for example, has type 1 diabetes rates 18 times lower than the United States. This disparity isn’t due only to genetics, however, because, when children migrate, they tend to acquire the risk of their new home, suggesting it’s got something to do with the environment, diet, or lifestyle. In fact, the incidence rates vary more than 350-fold around the world. Some countries have rates hundreds of times higher than others, and it is on the rise. Researchers looked at 37 populations from around the world and found that the incidence has been increasing about 3 percent a year—our genes don’t change that fast. In fact, they couldn’t find a single population with decreasing incidence of type 1 diabetes.

Something is going on that started around the end of World War II. “The best evidence available suggests that childhood diabetes [also known as type 1 diabetes] showed a stable and relatively low incidence over the first half of the 20th century, followed by a clear increase that began…around…the middle of the century.” Why the increase, though? A number of factors have been postulated, including vitamin D deficiency, certain infections, or exposure to cow’s milk.

Decades ago, published cross-country comparisons showed a tight correlation between milk consumption and the incidence of  type 1 diabetes. The “analysis showed that 94% of the geographic variation in incidence might be explained by differences in milk consumption.” Investigators in Finland, the country with the highest rates of type 1 diabetes and cow’s milk consumption, led much of the research into this area.

It all started with studies like the one I feature in my video Does Casein in Milk Trigger Type 1 Diabetes?, showing that the less babies are breastfed, the higher the rates of type 1 diabetes, leading to the obvious conclusion that “[b]reast-milk protects the newborn infant.” On the other hand, if babies are not getting breast milk, they’re getting formula, which probably contains cow’s milk proteins. In the first few months of life, our gut is especially leaky to proteins. Is it possible that as our immune system attacks the foreign cow proteins, our pancreas gets caught in the crossfire? This was based on animal experiments, however. In susceptible mice, a diet containing the cow’s milk protein, casein, produced diabetes, but it did not cause diabetes in rats. So, are we more like mice or rats?

Researchers drew blood from children with type 1 diabetes to see if they had elevated levels of antibodies that attack bovine proteins compared to controls. Their finding? Every single child with type 1 diabetes had elevated anti-bovine protein antibodies circulating in their blood compared to much lower levels in the control subjects. That seems pretty convincing, but what about Iceland? They drink more milk in Iceland than in Finland, yet Icelanders have less than half the type 1 diabetes. I explore this paradox in my follow-up video Does Bovine Insulin in Milk Trigger Type 1 Diabetes?.


The vast majority of diabetes cases are type 2, so that’s been my concentration:

I’m pleased to have been able to address type 1 diabetes. For even more on this disease, see:

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 Bariatric Surgery Reverses Diabetes

“Roux-en-Y gastric bypass surgery (RYGB) is one of the most successful treatment strategies for diabetes accompanying morbid obesity. Long-term diabetes remission rates of 83% have been reported.” These findings have led to the suggestion that the surgery improves diabetes by somehow altering digestive hormones, but this interpretation ignores the fact that patients are placed on a severely limited diet for a week or two after the operation just to recover from the major surgery. Severe caloric restriction alone can improve diabetes. So, is it the diet or the surgery?

To answer that question, researchers put diabetics on the exact same diet as one would eat post-RYGB surgery, with or without the actual surgery. As I discuss in Reversing Diabetes with Surgery, the researchers found that their diabetes improved rapidly on the surgery diet before they had the surgery. In fact, the improvement in blood sugar control was better on the diet alone than after the surgery.

Blood sugar control improved more in the absence of surgery.

This suggests that the whole surgical-diabetes-reversal is not due to the surgery at all, but rather because of the diet people have to go on in the hospital during recovery. So, the clinical implication is that nonsurgical interventions have just as much potential to resolve diabetes as major surgery does.

If you’re familiar with my video Diabetes as a Disease of Fat Toxicity, you’ll understand what is occurring. Namely, “[t]ype 2 diabetes can be understood as a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat”—that is, too much fat in the cells of the liver, pancreas, and muscles. Within seven days of eating about 600 calories a day by either dietary intervention or bariatric surgery, fasting glucose levels (blood sugar levels) can normalize, thanks to a fall in liver fat. If you look at CT scans, you can actually see a 35 percent reduction in liver volume as all the fat is cleared out. Then, the body starts pulling fat out of the pancreas. When the cause of diabetes goes away, the diabetes goes away.

The insulin-producing beta cells of the pancreas “had woken up!… Clearly, the [beta] cells are not permanently damaged in Type 2 diabetes, but are merely metabolically inhibited.” Studies show a reversal of diabetes up to 28 years after diagnosis.

So, diabetics enough to starve themselves can regain normal health. This information should be available to all people with type 2 diabetes, even though it is unlikely many will be motivated enough to escape from the disease. It’s not easy to not eat. Diabetics should know that if they don’t reverse their diabetes, their future health is in jeopardy, although the serious consequences must be balanced against the difficulties and privations associated with starvation diets. “For many people, this may prove too high a price to pay,” as it’s hard to voluntarily restrict food intake that much.

In that case, how about involuntary food restriction? That’s what stomach stapling surgery is. When you essentially remove someone’s stomach, they’re forced into compulsory food restriction.

Of course, major surgery carries major risks—during the operation and afterwards. There can be bleeding, leakage, infections, erosions, herniation, and severe nutritional deficiencies. Surgery or starvation? There has got to be a better way. And there is!

Instead of changing the quantity of food eaten, whether voluntarily or involuntarily, is it possible to reverse diabetes by changing the quality of the food? Watch my videos Reversing Diabetes with Food and Diabetes Reversal: Is It the Calories or the Food? to get the complete picture.


For the lowdown on saturated fat, check out Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Interested in taking a deeper dive into underlying causes of type 2 diabetes? You may be interested in these:

And, for an overview, see How Not to Die from 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, year-in-review presentations:

How to Treat the Root Cause of Diabetes

After about age 20, we may have all the insulin-producing beta cells we’re ever going to get. So if we lose them, we may lose them for good. Autopsy studies show that by the time type 2 diabetes is diagnosed, we may have already killed off half of our beta cells.

You can kill pancreatic cells right in a petri dish. If you expose the insulin-producing beta cells in our pancreas to fat, they suck it up and then start dying off. Fat breakdown products can interfere with the function of these cells and ultimately lead to their death. A chronic increase in blood fat levels can be harmful to our pancreas.

It’s not just any fat; it’s saturated fat. As you can see in my video, What Causes Diabetes?, predominant fat in olives, nuts, and avocados gives a tiny bump in death protein 5, but saturated fat really elevates this contributor to beta cell death. Therefore, saturated fats are harmful to beta cells. Cholesterol is, too. The uptake of bad cholesterol (LDL) can cause beta cell death as a result of free radical formation.

Diets rich in saturated fats not only cause obesity and insulin resistance, but the increased levels of circulating free fats in the blood (non-esterified fatty acids, or NEFAs) may also cause beta cell death and may thus contribute to the progressive beta cell loss we see in type 2 diabetes. These findings aren’t just based on test tube studies. When researchers have infused fat directly into people’s bloodstreams, they can show it directly impairing pancreatic beta cell function. The same occurs when we ingest it.

Type 2 diabetes is characterized by “defects in both insulin secretion and insulin action,” and saturated fat appears to impair both. Researchers showed saturated fat ingestion reduces insulin sensitivity within hours. The subjects were non-diabetics, so their pancreases should have been able to boost insulin secretion to match the drop in sensitivity. But no, “insulin secretion failed to compensate for insulin resistance in subjects who ingested [the saturated fat].” This implies saturated fat impaired beta cell function as well, again just within hours after going into our mouth. “[I]ncreased consumption of [saturated fats] has a powerful short- and long-term effect on insulin action,” contributing to the dysfunction and death of pancreatic beta cells in diabetes.

Saturated fat isn’t just toxic to the pancreas. The fats found predominantly in meat and dairy—chicken and cheese are the two main sources in the American diet—are considered nearly “universally toxic.” In contrast, the fats found in olives, nuts, and avocados are not. Saturated fat has been found to be particularly toxic to liver cells, contributing to the formation of fatty liver disease. If you expose human liver cells to plant fat, though, nothing happens. If you expose our liver cells to animal fat, a third of them die. This may explain why higher intake of saturated fat and cholesterol are associated with non-alcoholic fatty liver disease.

By cutting down on saturated fat consumption, we may be able to help interrupt these processes. Decreasing saturated fat intake can help bring down the need for all that excess insulin. So either being fat or eating saturated fat can both cause excess insulin in the blood. The effect of reducing dietary saturated fat intake on insulin levels is substantial, regardless of how much belly fat we have. It’s not just that by eating fat we may be more likely to store it as fat. Saturated fats, independently of any role they have in making us fat, “may contribute to the development of insulin resistance and its clinical consequences.” After controlling for weight, alcohol, smoking, exercise, and family history, diabetes incidence was significantly associated with the proportion of saturated fat in our blood.

So what causes diabetes? The consumption of too many calories rich in saturated fats. Just like everyone who smokes doesn’t develop lung cancer, everyone who eats a lot of saturated fat doesn’t develop diabetes—there is a genetic component. But just like smoking can be said to cause lung cancer, high-calorie diets rich in saturated fats are currently considered the cause of type 2 diabetes.

I have a lot of videos on diabetes, including:

Preventing the disease:

And treating it:

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: