Thu, Sep-03-15, 12:15
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Senior Member
Posts: 6,498
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Plan: VLC, mostly meat
Stats: 202/200/165
BF:
Progress: 5%
Location: Montreal, Quebec, Canada
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It gets complicated the longer I think about it. It's obvious insulin and BG are involved in both obesity and Alzheimer's. But it's not obvious how they're involved. According to my paradigm, obesity is easy to explain. The liver somehow can't degrade insulin fast enough, fasting insulin rises, fat tissue grows bigger. I think I got it. For Alzheimer's, the brain remains much more insulin sensitive, to in turn respond much more by degrading all that insulin on site, but with the same enzyme that otherwise works to degrade amyloid, which now accumulates instead. In both cases, the liver is resistant, it can't degrade insulin fast enough, fasting insulin rises, but the brain takes over the insulin-degrading with Alzheimer's, fasting insulin drops, fat tissue doesn't grow as big. However, keep that up and eventually the brain becomes resistant, can't degrade insulin as fast, fasting insulin rises again, fat tissue eventually grows bigger.
This gives me the idea that we can predict risk by determining where insulin is degraded most now. If the liver, then greater risk of future obesity. If the brain, then greater risk of future Alzheimer's. We could find out by looking at insulin-degrading enzyme activity in either tissue. Is this possible?
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