It may seem a bit too vague at first, but trust that we'll slowly start to increase our focus as we go. This point, that diabetes = inflammation, is an important one. Without it, we're floating in several directions all at once.
To discern that inflammation is the cause of Type I diabetes necessitates that there is a reason for the beta cells to become inflamed. I think all too often, people forget that inflammation is not a "thing" in and of itself. People are quick to medicate inflammation without understanding what is actually inflamed or questioning why.
Think of it like "gut health". How many times in the past week have you been told to improve your gut health? Eat yogurt, drink water, take probiotics... What exactly am I improving? It's an extremely broad stroke for a very specific problem.
For diabetics, zeroing in on inflammation and its source can help navigate away from some general ideas of how it came to be. There are a number of rabbit holes to go down. Most every Type I has a diagnosis story that includes several infections/illnesses/viruses that required antibiotic use. I personally suffered a long string of ear infections as a child, as well as two bouts with Lyme disease. This could lead one to believe that it could be an outside source, such as a viral insertion, to affect our genetic expression. It could also expose our bacterial composition as having a regulatory role in either our immune function or at the genetic level.
But those theories start to get fuzzy when you apply pressure. Both the viral and bacterial origin story behind diabetes require some serious scientific explanations. I am a man of simplicity. For either a virus or a specific ratio of bacteria to have such a pointed effect on just the pancreas and its beta cells is too much for me.
Back to the general idea of inflammation:
If there is inflammation and you don't know why it's there, what can you do to prevent it from happening again? You can have any solution you like, but you have no way to protect yourself. This is where stem cell and pancreatic transplant theories fall flat for me.
This goes back to the toxicology report that Type I diabetics never get. They find out beta cells are dead, but have no idea how it happened.
And while it may not be so simple to extricate and examine our inactive beta cells, I think that we can do a better job of triangulating some potential sources. This is why I've focused on the liver and spleen so much in previous posts. They deal with toxic substances and reactive material. They are neighbors with the pancreas. Is that really so far-fetched? It's like living next to the nuclear waste plant and wondering why all your house plants keep dying.
But what is it in the liver and spleen? What that they do leads to a common suspect?
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