Does Paratuberculosis in Meat Trigger Type 1 Diabetes?

Does Paratuberculosis in Meat Trigger Type 1 Diabetes?
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The majority of specialists in the field agreed that paraTB in meat and dairy likely represents a risk to human health and should be a high- or medium-priority public health issue.

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Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

The compelling finding of MAP bacteria circulating disproportionately within the bloodstream of type 1 diabetics was subsequently confirmed by culturing it straight out of their blood. But, just because being infected and type 1 diabetes appeared to go together, we don’t know what came first.

Yes, maybe the infection made kids more susceptible to diabetes. But, maybe the diabetes made kids more susceptible to infection. Maybe, this bug just likes hanging out in sugary blood. In that case, we might expect to see it in type 2 diabetics too. But no; paratuberculosis infection is not associated with type 2 diabetes—which would make sense, since type 2 is not an autoimmune disease.

For this infectious trigger idea to be sound, there would have to be an immune response mounted to the bug. And indeed, there is an extremely significant antibody response against paratuberculosis 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 mycobacterium paratuberculosis cross-react with the molecular signatures present on our insulin-producing beta cells in our pancreas.

Okay, but is this just in Sardinia? Or, might we find these same results elsewhere? The same results were found on mainland Italy, with a group of type 1 diabetics with different genetic backgrounds—a strong association between paraTB bacteria exposure and type 1 diabetes. And then, confirmed again, and again in other pediatric populations, as well as a group of type 1 diabetic adults.

The paratuberculosis bacteria also explain why type 1 diabetes risk is associated with a specific gene on chromosome 2, called SLC11A1. What does that gene do? It activates the immune cell that eats mycobacteria for breakfast. So, that could explain how a mutation in that gene could increase the susceptibility to type 1 diabetes—by increasing the “susceptibility to mycobacterial infections,” like mycobacterium avium paratuberculosis.

This is all part of this accumulating line of evidence pointing to MAP bacteria as a trigger for the development of type 1 diabetes. And, it’s 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. But, if our immune systems see through the disguise and start attacking the bacteria, our similar-looking proteins can become a victim of friendly fire, which is what these studies have all been pointing to. Or, almost all.

This 2015 review found that all seven out of seven human studies found an association between type 1 diabetes and paratuberculosis exposure. But, it’s actually only seven out of eight. Since that review, a study in India was published, finding no link. A few possible explanations were offered. Maybe it’s because they have compulsory vaccination for regular TB, which might offer cross-protection against paratuberculosis, as it does with leprosy. Or, maybe because they eat so much less meat.

Or, maybe it’s because of their “compulsory boiling of milk before consumption.” If you 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—though this may depend on the degree of fecal clumping. That may be one way MAP bacteria ride out pasteurization—by hiding in tiny fecal clumps. 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” how much MAP is in the milk, meat, and feces, and how much fecal material is in the milk and meat, to figure out what we need to do to kill it. In the meanwhile, what’s the potential public health impact of mycobacterium paratuberculosis? “The majority of specialists [in the field] agree that it’s likely a risk to human health and…[should be] a high- or medium-priority…public health issue. “

Please consider volunteering to help out on the site.

Image credit: Mark Doliner via flickr. Image has been modified.

Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

The compelling finding of MAP bacteria circulating disproportionately within the bloodstream of type 1 diabetics was subsequently confirmed by culturing it straight out of their blood. But, just because being infected and type 1 diabetes appeared to go together, we don’t know what came first.

Yes, maybe the infection made kids more susceptible to diabetes. But, maybe the diabetes made kids more susceptible to infection. Maybe, this bug just likes hanging out in sugary blood. In that case, we might expect to see it in type 2 diabetics too. But no; paratuberculosis infection is not associated with type 2 diabetes—which would make sense, since type 2 is not an autoimmune disease.

For this infectious trigger idea to be sound, there would have to be an immune response mounted to the bug. And indeed, there is an extremely significant antibody response against paratuberculosis 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 mycobacterium paratuberculosis cross-react with the molecular signatures present on our insulin-producing beta cells in our pancreas.

Okay, but is this just in Sardinia? Or, might we find these same results elsewhere? The same results were found on mainland Italy, with a group of type 1 diabetics with different genetic backgrounds—a strong association between paraTB bacteria exposure and type 1 diabetes. And then, confirmed again, and again in other pediatric populations, as well as a group of type 1 diabetic adults.

The paratuberculosis bacteria also explain why type 1 diabetes risk is associated with a specific gene on chromosome 2, called SLC11A1. What does that gene do? It activates the immune cell that eats mycobacteria for breakfast. So, that could explain how a mutation in that gene could increase the susceptibility to type 1 diabetes—by increasing the “susceptibility to mycobacterial infections,” like mycobacterium avium paratuberculosis.

This is all part of this accumulating line of evidence pointing to MAP bacteria as a trigger for the development of type 1 diabetes. And, it’s 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. But, if our immune systems see through the disguise and start attacking the bacteria, our similar-looking proteins can become a victim of friendly fire, which is what these studies have all been pointing to. Or, almost all.

This 2015 review found that all seven out of seven human studies found an association between type 1 diabetes and paratuberculosis exposure. But, it’s actually only seven out of eight. Since that review, a study in India was published, finding no link. A few possible explanations were offered. Maybe it’s because they have compulsory vaccination for regular TB, which might offer cross-protection against paratuberculosis, as it does with leprosy. Or, maybe because they eat so much less meat.

Or, maybe it’s because of their “compulsory boiling of milk before consumption.” If you 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—though this may depend on the degree of fecal clumping. That may be one way MAP bacteria ride out pasteurization—by hiding in tiny fecal clumps. 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” how much MAP is in the milk, meat, and feces, and how much fecal material is in the milk and meat, to figure out what we need to do to kill it. In the meanwhile, what’s the potential public health impact of mycobacterium paratuberculosis? “The majority of specialists [in the field] agree that it’s likely a risk to human health and…[should be] a high- or medium-priority…public health issue. “

Please consider volunteering to help out on the site.

Image credit: Mark Doliner via flickr. Image has been modified.

Doctor's Note

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.

If you haven’t yet, you can subscribe to my videos for free by clicking here.

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