Sputnik_Butts t1_j0rdlzm wrote

I think if you think about this with less bias you'll see the conclusions I see. You can be T1DM and have perfect control I suppose and never gain IR. But even perfect control won't prevent you from a tiny bit of wear and tear. You might not notice till you're 70 or 80, but by then everything will be significantly harder and the damage will add up faster.

I'm just saying as a T1, unless you're cured it's inevitable that we will get Alzheimer's even from micro adjustments. The only difference is what age we get it at.

Alzheimer's develops in healthy people without diabetes, you can't assume there's no risk for a T1. It's only logical that we have an increased risk, due to even a tiny IR gain.


Sputnik_Butts t1_j0ra5cf wrote

Then you should know that it's almost impossible to make it to 70y/o without a highblood sugar. The paper states that a large dose of insulin increases the risk of insulin resistance.

You should also know that low blood sugar damage and kills brain cells, which would imply cells with damaged functioning. If cells aren't functioning correctly how do you think they are going to respond to insulin efficiently?

I'm not saying near perfect control doesn't exist, but type 1 diabetics are at a significant risk to develop Alzheimer's. At least this paper is giving us more insight into the issue, and who knows maybe in the next 30 years we'll develop a way to repair cell receptors for insulin.


Sputnik_Butts t1_j0r0ugx wrote

"Type 1"s develop insulin resistance as well...

>"The existence of reduced tissue insulin sensitivity in children, adolescents, and adults diagnosed in T1DM is no longer being questioned. Our present analysis, which focused on IR in T1DM, presented that many factors influence the development of this disorder."

IR is insulin resistance.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7700208/


Sputnik_Butts t1_j0oes3w wrote

To add with a conclusion quote from the paper

>"Results of these experiments show that Alzheimer’s disease-like neuropathology impairs the activation of vascular INSRs in the 3xTg-AD mouse model. This collection of data indicates that circulating insulin primarily interacts with INSRs exposed on the luminal side of the BBB in both human and mice and that the INSR-mediated response is blunted in Alzheimer’s disease."

According to this research, it has been suggested that Alzheimer's disease may decrease the response of cells to insulin in both mice and humans, due to physiological similarities. The paper implies that the symptoms of Alzheimer's may not necessarily be caused by a deficiency in insulin, but rather by damage to the cells' ability to respond to it.

At least that's what I understood, I'm not a scientist for reference.