 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 which came first. Yes, maybe 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, but no, para tuberculosis 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 para tuberculosis 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 para tuberculosis 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 para TB 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 para tuberculosis bacteria also explains 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 para tuberculosis. All part of this accumulating line of evidence pointing to it 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 7 out of 7 human studies found an association between type 1 diabetes and para tuberculosis exposure, but it's actually only 7 out of 8. 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 para tuberculosis 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 might depend on the degree of fecal clumping. That may be one-way mapped bacteria write out pasteurization by hiding in tiny fecal clumps in milk. But only rarely should maps survive over 100 degrees Celsius, perhaps explaining the disparate India findings. Bottom line, to reduce human exposure to map via consumption of meat and dairy products, more studies are needed for estimating how much map there is in milk, meat, and feces, and how much feces 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 mycobacteria and para tuberculosis? 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.