So we've gone through a handful of (not so) new articles looking at the iron-glucose metabolism connection. Type II diabetics have been the "diabetics of choice" to study, presumably because of the preconceptions on its ability to be defended against.
This is opposed to the "loser of the genetic lottery" outlook the medical community has taken on Type I.
But I'm here to challenge that.
The more I've looked into iron the more potential for impact I see. I've come to realize that it might just be our beta-cell murderer.
About 2 years ago, I was introduced to the term "iron overload". Absent of any diabetic detective intuition, and there for health reasons related more to sports performance and physical training metrics, I had come across an alternative health community highlighting this iron overload as a foundational cause of much of today's autoimmune dysfunction.
The focus was on the effects of balancing vitamins and minerals to help maximize your natural iron recycling ability. They cited experience healing conditions and disorders like PCOS, celiac, IBS and anemia.
Sounds good. Is this like a detox thing? I see those conditions and think of them as less than diabetes on the Richter Scale of chronic conditions (just my ego flexing). Call me a purist.
But the introduction to the idea of iron overload was enough to plant a seed. I didn't act immediately. I continued to lift weights and slowly adapted the eating habits outlined in the protocol. Energy was up, sleep was improving so I was pleased.
So what even is iron overload and does it leave any clues in and around the beta cell crime scene?
Simply put, iron overload is defined as excess stores of iron in the body. Makes sense.
Whether dietary, environmental or related to some genetic impairment, there's too much iron in circulation and it cannot be safely managed by the body any longer.
There's actually a heritable condition related to this. It's called hemochromatosis.
This condition is what has lit my research fire. An interesting fact I learned about hemochromatosis patients? Over 50% of them develop Type I and Type II diabetes.
> 50%
How much more to do I need to say? Type I and Type II. Citations and clinical findings dating back to mid-19th century.
How have we missed this? Does your endocrinologist really not know about this?
If there's this much in the research, how much further does it go?
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