The Crowding Out Strategy to Eating Healthier

It may be more expedient politically to promote an increase in consumption of healthy items rather than a decrease in consumption of unhealthy items, but it may be far less effective.

The World Health Organization has estimated that more than a million deaths “worldwide are linked to low fruit and vegetable consumption.” What can be done about it? I explore this in my video Is it Better to Advise More Plants or Less Junk?

There’s always appealing to vanity. A daily smoothie can give you a golden glow as well as a rosy glow, both of which have been shown to “enhance healthy appearance” in Caucasian, Asian, and African skin tones, as you can see at 0:24 in my video.

What about giving it away for free?

A free school fruit scheme was introduced in Norway for grades 1 through 10. Fruit consumption is so powerfully beneficial that if kids ate only an additional 2.5 grams of fruit a day, the program would pay for itself in terms of saving the country money. How much is 2.5 grams? The weight of half of a single grape. However, that cost-benefit analysis assumed this minuscule increased fruit consumption would be retained through life. It certainly seemed to work while the program was going on, with a large increase in pupils eating fruit, but what about a year after the free fruit program ended? The students were still eating more fruit. They were hooked! Three years later? Same thing. Three years after they had stopped getting free fruit, they were still eating about a third of a serving more, which, if sustained, is considerably more than necessary for the program to pay for itself.

There were also some happy side effects, including a positive spillover effect where not only the kids were eating more fruit, but their parents started eating more, too. And, although the “intention of these programs was not to reduce unhealthy snack intakes,” that’s exactly what appeared to happen: The fruit replaced some of the junk. Increasing healthy choices to crowd out the unhealthy ones may be more effective than just telling kids not to eat junk, which could actually backfire. Indeed, when you tell kids not to eat something, they may start to want it even more, as you can see at 2:20 in my video.

Which do you think worked better? Telling families to increase plants or decrease junk? Families were randomly assigned to one of two groups, either receiving encouragement to get at least two servings of fruits and veggies a day, with no mention of decreasing junk, or being encouraged to get their junk food intake to less than ten servings a week, with no mention of eating more fruits and veggies. What do you think happened? The Increase Fruit and Vegetable intervention just naturally “reduced high-fat/high-sugar intake,” whereas those in the Decrease Fat and Sugar group cut back on junk but didn’t magically start eating more fruits and vegetables.

This crowding out effect may not work on adults, though. As you can see at 3:12 in my video, in a cross-section of over a thousand adults in Los Angeles and Louisiana, those who ate five or more servings of fruits and veggies a day did not consume significantly less alcohol, soda, candy, cookies, or chips. “This finding suggests that unless the excessive consumption of salty snacks, cookies, candy, and sugar-sweetened beverages”—that is, junk—“is curtailed, other interventions…[may] have a limited impact….It may be politically more expedient to promote an increase in consumption of healthy items rather than a decrease in consumption of unhealthy items, but it may be far less effective.” In most public health campaigns, “messages have been direct and explicit: don’t smoke, don’t drink, and don’t take drugs.” In contrast, food campaigns have focused on eat healthy foods rather than cut out the crap. “Explicit messages against soda and low-nutrient [junk] foods are rare.”

In the United States, “if one-half of the U.S. population were to increase fruit and vegetable consumption by one serving each per day, an estimated 20,000 cancer cases might be avoided each year.” That’s 20,000 people who would not have gotten cancer had they been eating their fruits and veggies. The U.S. Department of Agriculture recommends we “fill half [our] plate with colorful fruits and vegetables,” but less than 10 percent of Americans hit the recommended daily target. Given this sorry state of affairs, should we even bother telling people to strive for “5 a day,” or might just saying “get one more serving than you usually do” end up working better? Researchers thought that “the more realistic ‘just 1 more’ goal would be more effective than the very ambitious ‘5 a day’ goal,” but they were wrong.

As you can see at 4:56 in my video, those told to eat one more a day for a week, ate about one more a day for a week, and those told to eat five a day for a week did just that, eating five a day for a week. But here’s the critical piece: One week after the experiment was over, the group who had been told to eat “5 a day” was still eating about a serving more, whereas the “just 1 more” group went back to their miserable baseline. So, more ambitious eating goals may be more motivating. Perhaps this is why “in the US ‘5 a day’ was replaced by the ‘Fruits and Veggies—More Matters’ campaign…in which a daily consumption of 7–13 servings of fruits and vegetables – FVs –  is recommended.” However, if the recommendation is too challenging, people may just give up. So, instead of just sticking with the science, policy makers evidently need to ask themselves questions like “How many servings are regarded as threatening?”


For more on appealing to vanity to improve fruit and vegetable consumption, see my videos Eating Better to Look Better and Beauty Is More Than Skin Deep.

What does the science say about smoothies? See:

The flipside of free fruit programs is to tax instead of subsidize. Learn more by checking out my video Would Taxing Unhealthy Foods Improve Public Health?

For more on the paternalistic attitude that you don’t care enough about your health to be told the truth, see my videos Everything in Moderation? Even Heart Disease? and Optimal Diet: Just Give It to Me Straight, Doc.

I explore this same patronizing attitude when it comes to physical activity in How Much Should You Exercise?

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:

 

What Happens if You Have Red Wine or Avocados with a Meal?

Whole plant sources of sugar and fat can ameliorate some of the postprandial (after meal) inflammation caused by the consumption of refined carbohydrates and meat.

Studies have shown how adding even steamed skinless chicken breast can exacerbate the insulin spike from white rice, but fish may be worse. At 0:18 in my video The Effects of Avocados and Red Wine on Meal-Induced Inflammation, you can see how the insulin scores of a low-carbohydrate plant food, peanuts, is lower compared to common low-carb animal foods—eggs, cheese, and beef. Fish was even worse, with an insulin score closer to doughnut territory.

At 0:36 in my video, you can see the insulin spike when people are fed mashed white potatoes. What do you think happens when they’re also given tuna fish? Twice the insulin spike. The same is seen with white flour spaghetti versus white flour spaghetti with meat. The addition of animal protein may make the pancreas work twice as hard.

You can do it with straight sugar water, too. If you perform a glucose challenge to test for diabetes, drinking a certain amount of sugar, at 1:10 in my video, you can see the kind of spike in insulin you get. But, if you take in the exact same amount of sugar but with some meat added, you get a higher spike. And, as you can see at 1:25 in my video, the more meat you add, the worse it gets. Just adding a little meat to carbs doesn’t seem to do much, but once you get up to around a third of a chicken’s breast worth, you can elicit a significantly increased surge of insulin.

So, a chicken sandwich may aggravate the metabolic harm of the refined carb white bread it’s on, but what about a PB&J? At 1:49 in my video, you can see that adding nuts to Wonder Bread actually calms the insulin and blood sugar response. What if, instead of nuts, you smeared on an all fruit strawberry jam? Berries, which have even more antioxidants than nuts, can squelch the oxidation of cholesterol in response to a typical American breakfast and even reduce the amount of fat in your blood after the meal. And, with less oxidation, there is less inflammation when berries are added to a meal.

So, a whole plant food source of sugar can decrease inflammation in response to an “inflammatory stressor” meal, but what about a whole plant food source of fat? As you can see at 2:38 in my video, within hours of eating a burger topped with half an avocado, the level of an inflammatory biomarker goes up in your blood, but not as high as eating the burger without the avocado. This may be because all whole plant foods contain antioxidants, which decrease inflammation, and also contain fiber, which is one reason even high fat whole plant foods like nuts can lower cholesterol. And, the same could be said for avocados. At 3:12 in my video, you can see avocado causing a significant drop in cholesterol levels, especially in those with high cholesterol, with even a drop in triglycerides.

If eating berries with a meal decreases inflammation, what about drinking berries? Sipping wine with your white bread significantly blunts the blood sugar spike from the bread, but the alcohol increases the fat in the blood by about the same amount. As you can see at 3:40 in my video, you’ll get a triglycerides bump when you eat some cheese and crackers, but if you sip some wine with the same snack, triglycerides shoot through the roof. How do we know it was the alcohol? Because if you use dealcoholized red wine, the same wine but with the alcohol removed, you don’t get the same reaction. This has been shown in about a half dozen other studies, along with an increase in inflammatory markers. So, the dealcoholized red wine helps in some ways but not others.

A similar paradoxical effect was found with exercise. If people cycle at high intensity for about an hour a half-day before drinking a milkshake, the triglycerides response is less than without the prior exercise, yet the inflammatory response to the meal appeared worse, as you can see at 4:18 in my video. The bottom line is not to avoid exercise but to avoid milkshakes.

The healthiest approach is a whole food, plant-based diet, but there are “promising pharmacologic approaches to the normalization” of high blood sugars and fat by taking medications. “However, resorting to drug therapy for an epidemic caused by a maladaptive diet is less rational than simply realigning our eating habits with our physiological needs.”

Protein from meat can cause more of an insulin spike than pure table sugar. See the comparisons in my video Paleo Diets May Negate Benefits of Exercise.

Interested in more information on the almond butter study I mentioned? I discuss it further in How to Prevent Blood Sugar and Triglyceride Spikes After Meals.

Berries have their own sugar, so how can eating berries lower the blood sugar spike after a meal? Find out in If Fructose Is Bad, What About Fruit?


For more on avocados, check out:

And here are more videos on red wine:

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:

Decreasing Inflammation and Oxidation After Meals

Within hours of eating an unhealthy meal, we can get a spike in inflammation, crippling our artery function, thickening our blood, and causing a fight-or-flight nerve response. Thankfully, there are foods we can eat at every meal to counter this reaction.

Standard American meals rich in processed junk and meat and dairy lead to exaggerated spikes in sugar and fat in the blood, as you can see at 0:13 in my video How to Prevent Blood Sugar and Triglyceride Spikes after Meals. This generates free radicals, and the oxidative stress triggers a biochemical cascade throughout our circulation, damaging proteins in our body, inducing inflammation, crippling our artery function, thickening our blood, and causing a fight-or-flight nerve response. This all happens within just one to four hours after eating a meal. Worried about inflammation within your body? One lousy breakfast could double your C-reactive protein levels before it’s even lunchtime.

Repeat that three times a day, and you can set yourself up for heart disease. You may not even be aware of how bad off you are because your doctor is measuring your blood sugar and fat levels while you’re in a fasting state, typically drawing your blood before you’ve eaten. What happens after a meal may be a stronger predictor of heart attacks and strokes, which makes sense, since this is where most of us live our lives—that is, in a fed state. And it’s not just in diabetics. As you can see at 1:30 in my video, if you follow non diabetic women with heart disease but normal fasting blood sugar, how high their blood sugar spikes after chugging some sugar water appears to determine how fast their arteries continue to clog up, perhaps because the higher the blood sugars spike, the more free radicals are produced.

So, what are some dietary strategies to improve the situation? Thankfully, “improvements in diet exert profound and immediate favorable changes…,” but what kind of improvements? “Specifically, a diet high in minimally processed, high-fiber, plant-based foods such as vegetables and fruits, whole grains, legumes, and nuts,”—antioxidant, anti-inflammatory whole plant foods—“will markedly blunt the post-meal increase” in sugar, fat, and inflammation.

But what if you really wanted to eat some Wonder Bread? As you can see at 2:23 in my video, you’d get a big spike in blood sugar less than an hour after eating it. Would it make a difference if you spread the bread with almond butter? Adding about a third of a cup of almonds to the same amount of Wonder Bread significantly blunts the blood sugar spike.

In that case, would any low-carb food help? Why add almond butter when you can make a bologna sandwich? Well, first of all, plant-based foods have the antioxidants to wipe out any excess free radicals. So, nuts can not only blunt blood sugar spikes, but oxidative damage as well. What’s more, they can even blunt insulin spikes. Indeed, adding nuts to a meal calms both blood sugar levels and insulin levels, as you can see at 3:02 in my video. Now, you’re probably thinking, Well, duh, less sugar means less insulin, but that’s not what happens with low-carb animal foods.

As you can see at 3:23 in my video, if you add steamed skinless chicken breast to your white rice, you get a greater insulin spike than if you had just eaten the white rice alone. So, adding the low-carb plant food made things better, but adding the low-carb animal food made things worse. It’s the same with adding chicken breast to mashed potatoes—a higher insulin spike with the added animal protein. It is also the same with animal fat: Add some butter to a meal, and get a dramatically higher insulin spike from some sugar, as you can see at 3:45 in my video.

If you add butter and cheese to white bread, white potatoes, white spaghetti, or white rice, you can sometimes even double the insulin reaction. If you add half an avocado to a meal, however, instead of worsening, the insulin response improves, as it does with the main whole plant food source of fat: nuts.


I’ve covered the effect adding berries to a meal has on blood sugar responses in If Fructose Is Bad, What About Fruit?, and that raises the question: How Much Fruit Is Too Much?

In addition to the all-fruit jam question, I cover The Effects of Avocados and Red Wine on Postprandial Inflammation.

Vinegar may also help. See Can Vinegar Help with Blood Sugar Control?.

Perhaps this explains part of the longevity benefit to nut consumption, which I discuss in Nuts May Help Prevent Death.

I also talk about that immediate inflammatory reaction to unhealthy food choices in Best Foods to Improve Sexual Function.

Surprised by the chicken and butter reaction? The same thing happens with tuna fish and other meat, as I cover in my video Paleo Diets May Negate Benefits of Exercise.

Also check:

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:

 

Does Aspartame Cause Lymphoma?

The approval of aspartame has a controversial history. The Commissioner of the U.S. Food and Drug Administration (FDA) concluded that “there is a reasonable certainty that human consumption of aspartame: (1) …will not pose a risk of brain damage resulting in mental retardation, endocrine [hormonal] dysfunction, or both; and (2) will not cause brain tumors.” However, the FDA’s own Public Board of Inquiry withdrew their approval over cancer concerns. “Further, several FDA scientists advised against the approval of aspartame, citing…[the aspartame company’s] own brain tumor tests…” Regardless, the Commissioner approved aspartame before he left the FDA and went on to enjoy a thousand-dollar-a-day consultancy position with the aspartame company’s PR firm. Then, the FDA actually prevented the National Toxicology Program (NTP) from doing further cancer testing. As I discuss in my video Does Aspartame Cause Cancer? we were then left with people battling over different rodent studies, some of which showed increased cancer risk, while others didn’t.

This reminds me of the saccharin story. That artificial sweetener caused bladder cancer in rats but not mice, leaving us “to determine whether humans are like the rat or like the mouse.” Clearly, we had to put the aspartame question to the test in people, but the longest human safety study lasted only 18 weeks. We needed better human data.

Since the largest rat study highlighted lymphomas and leukemias, the NIH-AARP study tracked blood cancer diagnoses and found that “[h]igher levels of aspartame intake were not associated with the risk of…cancer.” Although the NIH-AARP study was massive, it was criticized for only evaluating relatively short-term exposure. Indeed, people were only studied for five years, which is certainly better than 18 weeks, but how about 18 years?

All eyes turned to Harvard, where researchers had started following the health and diets of medical professionals before aspartame had even entered the market. “In the most comprehensive long-term [population] study…to evaluate the association between aspartame intake and cancer risk in humans,” they found a “positive association between diet soda and total aspartame intake and risks of [non-Hodgkin’s lymphoma] and multiple myeloma in men and leukemia in both men and women,” as you can see at 2:12 in my video. Why more cancer in men than women? A similar result was found for pancreatic cancer and diet soda, but not soda in general. In fact, the only sugar tied to pancreatic cancer risk was the milk sugar, lactose. The male/female discrepancy could have simply been a statistical fluke, but the researchers decided to dig a little deeper.

Aspartame is broken down into methanol, which is turned into formaldehyde, “a documented human carcinogen,” by the enzyme alcohol dehydrogenase.The same enzyme that detoxifies regular alcohol is the very same enzyme that converts methanol to formaldehyde. Is it possible men just have higher levels of this enzyme than women? Yes, which is why women get higher blood alcohol levels than men drinking the same amount of alcohol. If you look at liver samples from men and women, you can see significantly greater enzyme activity in the men, so perhaps the higher conversion rates from aspartame to formaldehyde explain the increased cancer risk in men? How do we test this?

Ethanol—regular alcohol—competes with methanol for this same enzyme’s attention. In fact, regular alcohol is actually “used as an antidote for methanol poisoning.” So, if this formaldehyde theory is correct, men who don’t drink alcohol or drink very little may have higher formaldehyde conversion rates from aspartame. And, indeed, consistent with this line of reasoning, the men who drank the least amounts of alcohol appeared to have the greatest cancer risk from aspartame.

A third cohort study has since been published and found no increased lymphoma risk associated with diet soda during a ten-year follow-up period. So, no risk was detected in the 18-week study, the 5-year study, or the 10-year study—only in the 18-year study. What should we make of all this?

Some have called for a re-evaluation of the safety of aspartame. The horse is kind of out of the barn at this point with 34 million pounds of aspartame produced annually, but that doesn’t mean we have to eat it, especially, perhaps, pregnant women and children.


For more information on the effects of aspartame, watch my videos Aspartame and the Brain and Aspartame-Induced Fibromyalgia. Interested in learning more about the effects of consuming diet soda? See, for example:

What about Splenda? Or monk fruit sweetener? I have videos on those, too—watch Effect of Sucralose (Splenda) on the Microbiome and Is Monk Fruit Sweetener Safe?.

I also do a comparison of the most popular sweeteners on the market, including stevia and xylitol, in my video A Harmless Artificial Sweetener.

Perhaps the best candidate is erythritol, which you can learn about in my video Erythritol May Be a Sweet Antioxidant. That said, it’s probably better if we get away from all intense sweeteners, artificial or not. See my video Unsweetening the Diet for more on this.

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 to Prevent the Infection that May Trigger Type 1 Diabetes

The compelling finding of Mycobacterium avium paratuberculosis (MAP) circulating disproportionately within the bloodstream of type 1 diabetics was subsequently confirmed by culturing it straight out of their blood. MAP infection and type 1 diabetes appear to go together, but we didn’t know which came first. Does the infection make kids more susceptible to diabetes? Might diabetes make kids more susceptible to infection? Maybe this MAP bug just likes hanging out in sugary blood. In that case, we might expect to also see it in type 2 diabetics, but, no: Paratuberculosis infection is not associated with type 2 diabetes, which makes sense since type 2 is not an autoimmune disease.

In order for the idea of MAP infection triggering type 1 diabetes to be sound, there would have to be an immune response mounted to the bug, and, indeed, there is. Researchers in Sardinia found an “extremely significant” antibody response against paratuberculosis (paraTB) bacteria in type 1 diabetics. But do the antibodies attacking the bug cross-react with our own insulin-producing cells to generate that autoimmune reaction? Apparently so. Antibodies recognizing the molecular signatures of MAP cross-react with the molecular signatures present on our insulin-producing beta cells in the pancreas, as you can see at 1:09 in my video Does Paratuberculosis in Meat Trigger Type 1 Diabetes?.

Is this just in Sardinia, or might we find these same results elsewhere? The same results were in fact found on mainland Italy with a group of type 1 diabetics “with a genetic background different from Sardinians”—a strong association between paraTB bacteria exposure and type 1 diabetes. The findings were confirmed in further studies, confirmed once more in other pediatric populations, and confirmed in a group of type 1 diabetic adults, as well.

The paratuberculosis bacterium may also explain why type 1 diabetes risk is associated with a specific gene on chromosome 2 called SLC11A1. What does that gene do? SLC11A1 activates the immune cell that eats mycobacteria for breakfast. This could explain how a mutation in that gene could increase the susceptibility to type 1 diabetes—namely, by increasing the susceptibility to mycobacterial infections, like Mycobacterium avium paratuberculosis. Indeed, an “[a]ccumulating line of evidence points…[to] MAP in the development of T1DM [type 1 diabetes] as an environmental trigger.” It’s likely no coincidence. These types of bacteria have evolved to disguise themselves to look like human proteins for the express purpose of avoiding detection by our immune system. These are not the droids you’re looking for. If, however, our immune system sees through the disguise and starts attacking the bacteria, our similar-looking proteins can become a victim of friendly fire, which is what nearly all of these studies have been pointing to. Nearly, but not all.

A 2015 review found that seven out of seven human studies found an association between type 1 diabetes and paratuberculosis exposure, but it’s actually seven out of eight. Since that review came out, a study in India was published finding no link. A few possible explanations were offered. Maybe it’s because vaccination for regular TB is compulsory in India, which might offer “cross protection from MAP as in case of leprosy,” or because they eat so much less meat due to “certain cultural and culinary practices such as widespread vegetarianism,” or because of their “compulsory boiling of milk before consumption…” If we measure the heat inactivation of milk with high concentrations of naturally infected feces, which is probably the main source of milk contamination, pasteurization may not completely inactivate the bacteria, but sterilization at boiling temperatures should (as you can see at 3:40 in my video). This may depend on the degree of fecal clumping, though. MAP bacteria may be able to ride out pasteurization by hiding in tiny fecal clumps in milk, but only rarely should MAP survive over 100 degrees Celsius, perhaps explaining the disparate India findings. 

Bottom line: “To reduce human exposure to MAP via consumption of dairy and meat products…[more] studies are needed for estimating the amount of MAP” in milk, meat, and feces, as well as “the amount of faecal contamination of milk and carcasses [meat]” to figure out what we need to do to kill it. In the meanwhile, what’s the potential public health impact of Mycobacterium avium paratuberculosis? The majority of specialists in the field agree that it “is likely a risk to human health” and should be “a high- or medium-priority…public health issue.” 


I started speaking out about the link between human disease and paratuberculosis infection in milk and meat 15 years ago. As cynical as I can be at times, even I am shocked that the industry hasn’t done more to clean up its act. It reminds me of the bovine leukemia virus story. See:

If you missed the first two installments in this series, check out Does Paratuberculosis in Milk Trigger Type 1 Diabetes? and Meat Consumption and the Development of Type 1 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:

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.

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