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Glucose Deprivation In The Brain Is A Causative Factor In Alzheimer's Dieases (AD)

Discussion in 'Scientific Studies' started by haidut, Feb 10, 2017.

  1. haidut

    haidut Member

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    As the study says, whether lower glucose levels in the brain were the consequence or cause of AD was considered unknown until recently. This is one of the studies that established a causal link between lower blood glucose levels in the brain and the development AD. I wonder if we are going to see an epidemic of AD in the coming years due to the massive marketing of the new "blockbuster" glucose-lowering drugs known as the *glitazones. They are already known to cause cancer and pancreatitis, and now AD can probably be added to their list of "acceptable" side effects. But the more important message is that after 50 years of claiming that AD is a genetic disease mainstream medicine is finally beginning to admit that something as mundane as diet (and lifestyle) could be the cause of AD.

    Glucose deprivation in the brain sets stage for Alzheimer's disease, Temple study shows

    "...One of the earliest signs of Alzheimer's disease is a decline in glucose levels in the brain. It appears in the early stages of mild cognitive impairment -- before symptoms of memory problems begin to surface. Whether it is a cause or consequence of neurological dysfunction has been unclear, but new research at the Lewis Katz School of Medicine at Temple University now shows unequivocally that glucose deprivation in the brain triggers the onset of cognitive decline, memory impairment in particular."

    "...The findings also lend support to the idea that chronically occurring, small episodes of glucose deprivation are damaging for the brain. "There is a high likelihood that those types of episodes are related to diabetes, which is a condition in which glucose cannot enter the cell," he explained. "Insulin resistance in type 2 diabetes is a known risk factor for dementia."
     
  2. tca300

    tca300 Member

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    Very interesting! Thank you!
     
  3. Tarmander

    Tarmander Member

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    I have seen some glitazone usage, but it seems to me a lot of endocrinologists are getting into the GLP-1 agonists (victoza, trulicity, etc), which causes an increase in insulin secretion apparently.

    You think these might fall into the same AD trap?
     
  4. OP
    haidut

    haidut Member

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    They have the same side effects - pancreatitis and cancer, which shows that messing with glucose levels directly is probably not a good idea.
     
  5. Mary Pruter

    Mary Pruter Member

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    My mother has dementia and her blood sugar is normal, 95, when she hasn't had food but once she eats her sugar goes up to almost 400. When I told her doctor about that he said, well, she just ate. Isn't that a very high reading even if she just ate? I have diabetes and if I eat my sugar goes up to 256.
     
  6. Mary Pruter

    Mary Pruter Member

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    Haidut, I need to email you and I'm new here and having a hard time figuring things out here!
    Mpruter77@gmail.com
     
  7. Westside PUFAs

    Westside PUFAs Member

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    Of course. The brain is a large, bulbous, out of proption protrusion from our spinal column that needs a lot of sugar daily. Even when in deep ketosis and burning lots of ketone bodies on a water only fast, it still needs some glucose.
     
  8. OP
    haidut

    haidut Member

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  9. Mary Pruter

    Mary Pruter Member

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    Thank you.
     
  10. bzmazu

    bzmazu Member

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    Thanks for more good info!
     
  11. Peater Piper

    Peater Piper Member

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    Paymanz started a similar thread here:

    Brain Insulin Resistance Identified As Possible New Link Between Alzheimer's Disease, Diabetes

    The glucose is probably there, but the brain can't utilize it due to insulin resistance within the brain. This study even goes so far to suggest that it may be the impaired insulin signaling in the hypothalamus that leads to diabetes in the first place:

    http://www.alzheimersanddementia.com/article/S1552-5260(16)00049-2/fulltext
    https://www.sciencedaily.com/releases/2016/04/160407221709.htm

     
  12. OP
    haidut

    haidut Member

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    Over the last 5 or so years Alzheimer has been called diabetes type III or "brain diabetes" among some "rogue" endocrinologists. This of course suggests FFA (PUFA) overload, which has been confirmed in other studies.
    Increased Pufa Oxidation May Be Biomarker For Alzheimers
    Blocking PUFA Metabolism May Reverse Alzheimer Disease (AD)
    Alzheimer Disease (AD) Is Likely A Metabolic Disorder
     
  13. Mary Pruter

    Mary Pruter Member

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    I must be doing something very wrong. Day 5 of 250+ mornings are much lower, 205 but all day it's too high.
     
  14. johnwester130

    johnwester130 Member

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    How would someone in the modern world become "glucose deficient" ?
     
  15. OP
    haidut

    haidut Member

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    By relying too much on fatty acid oxidation, which happens when you are under constant stress. Anf if enough of that fat is PUFA then you get the inflammatory derivatives, which are known to cause AD directly. Look at the 3 links I posted in response to Peater. Niacinamide reportedly succeeded in stopping the progression of AD in a human clinical trial for that reason - inhibiting both lipolysis and fatty acid oxidation.
    Safety Study of Nicotinamide to Treat Alzheimer's Disease - Full Text View - ClinicalTrials.gov
     
  16. SAFarmer

    SAFarmer Member

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    "Pseudohypoxia"

    Someone has read the latest Ray Peat Newsletter ...
     
  17. Peater Piper

    Peater Piper Member

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  18. OP
    haidut

    haidut Member

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    I emailed the lead author. He said he cannot disclose full results but he was very excited and the results went way beyond the simple toxicity study he aimed for this to be. I asked if he would take niacinamide if he was diagnosed with AD and he answered "yes!". They may delay publication because apparently UCI is working on a patentable niacinamide version based on the results of the study. So, they want to be able to license an actual drug to a pharma company if the full results are indeed front-page news.
     
  19. Mary Pruter

    Mary Pruter Member

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    You are saying it stops it but are any studies of this showing it reversing, our patients improving and how long does it take?
     
  20. Peater Piper

    Peater Piper Member

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    I can understand them wanting to make a profit, but that sounds really unethical to not release the information for a treatment that could potentially help current Parkinson's sufferers.
     
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