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BafangFan t1_j3g5mdf wrote

We spend so much time and money barking up the wrong tree.

Alzheimer's is called by some researchers as Type 3 Diabetes. That indicates there is a glucose metabolism impairment in the system.

Even back in 2019 they found that scanning the brain for glucose metabolism was more accurate at predicting Alzheimer's than scanning for amyloid plaques.

https://www.beingpatient.com/alzheimers-pet-scans/

The brain can run on glucose, but it can also run on fat and ketones. And both fat and ketones can ameliorate the issue of glucose metabolism impairment.

There is a growing body of anecdotal data to show improvement in Alzheimer's and dementia symptoms in people who follow a carnivore or ketogenic diet. A clinical ketogenic diet is also a standard of care in drug resistant epilepsy in children - so it's already a medically approved technique for brain impairment issues.

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calumin t1_j3hrjep wrote

Given that the data is anecdotal, you might be barking up the wrong tree. Still, it’s worth spending some time and money investigating it.

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BafangFan t1_j3i4zu0 wrote

Yeah, I/we could be wrong.

But the risks of diet change are very low. Maybe so diarrhea and cravings in the early stages of transition. Maybe some boredom of a limited diet.

But the rewards can be significant. People have gone from living in Groundhogs Day to being able to remember the past few months.

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calumin t1_j3i6qjq wrote

Ok but this post about the science related to something completely different.

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BafangFan t1_j3ie4jf wrote

I thought it was about the science of how to detect the degree of Alzheimer's in a person ?

I'm arguing that glucose metabolism is a more insightful indicator of Alzheimer's progression than any plaques/proteins.

And I'm arguing that if glucose metabolism is functioning poorly, the brain can alternatively use more fat/ketones; and with a non-impaired fuel source metabolism, the brain can restore some of its previous function.

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calumin t1_j3imrll wrote

That’s not what the scientific article is about.

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BafangFan t1_j3j4jkx wrote

>Rather than Alzheimer’s simply involving increased production of Aβ protein, the more important issue may be a reduced ability to effectively clear the protein and stave off the creation of plaque-contributing fibrillary amyloid, Thorwald said.

>“These findings further support the use of aggregated, or fibrillary, amyloid as a biomarker for Alzheimer’s treatments,” Thorwald said. “The site in which amyloid processing occurs has less precursor and enzyme available for processing, which may suggest the removal of amyloid as a key issue during Alzheimer’s.”

The focus is still on amyloid plaques, is it not?

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