Iron Has Direct Ties to the Pancreas
Updated: Dec 20, 2022
We've found iron in a litigious situation with diabetes, with historical ties to both Type 1 and 2.
Those with high serum ferritin (the iron-storage protein) are significantly more likely to develop diabetes than those with low ferritin levels. The speculation on the actual pathology of the disease itself ranges from targeted oxidative stress to tissue fibrosis.
Iron, it turns out, can be a nasty element. The single most abundant element on earth, even more than oxygen, it's celebrated for its toughness (the earth's core, axes, the toe box of your boots). But how does that translate when you start to infuse it into your body tissues?
Not well. Iron is incredibly reactive with both water and oxygen (I.e. rust). Reactive oxygen species (ROS) are at the very core of most of today's age-related diseases. Oxygen in the body reacts poorly with certain compounds, whose byproducts become toxic to the tissues and cells.The greatest source of the ROS, you may wonder? Unbound iron.
So when I learned of the correlation between iron, oxidative stress and diabetes, the crime scene that is my diabetic body started to materialize.
From observations as far back as the mid-1800s, doctors and scientists have noted the resulting fibrosis in those with high iron levels. Turns out 1850s doctors would dissect and stain the tissues of the deceased for iron to see where it had accumulated. Thick, less pliable tissues meant fibrosis. And what were the organs most heavily stained with iron? The liver and the pancreas.
One not so surprising, the other significantly so. Iron in the liver makes sense, as
it is where iron is stored and is the main site of iron recycling. On the other hand, I'm pretty sure the pancreas isn't supposed to have a lot, if any.
What gives? Is there anything in the past two centuries on that?
There are a few, especially recently. Here's are a few tidbits from my search:
From a 2021 paper
Iron-mediated beta-cell toxicity is mainly due to reactive oxygen species (ROS) accumulation through Fenton’s reaction. ROS excess determines DNA, lipid and protein oxidation that causes mitochondrial damage, leading to insulin release and apoptosis (1)
2. From a 2019 paper
In this study, we focused on the role of low hepcidin level-induced increased iron deposition in β-cells and the relationship between abnormal iron metabolism and β-cell dysfunction.
This...this is the answer we're looking for, no? Increased iron leads to ROS which kills beta cells. This is the cause of Type I diabetes.
This is the cause of Type I diabetes. And in 2019 and 2021? That's almost two years ago. Why aren't we talking about this?
I am in disbelief of how few people are talking about this.