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

[Mary Pruter]

That is sad! And, I'm sure once the drug companies get ahold of it, they'll mess it up!

 

[johnwester130]

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

Is a liquid glucose product coming ?

 

[haidut]

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.

I know, but it is very common. As another forum user mentioned before, there was a 5-Ht1 antagonist that completed successfully all stages of clinical trials and yet was never released as a drug and the studies on the trials were never published. We know it was successful because the govt site says so, but the company is mum on why they did not proceed with an actual new drug application or what the best dose in the study was. If a company pays for a trial they can do whatever they want with the results, including hiding them forever. There are no ethics laws that can compel them to release the data.

 

[haidut]

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

The human study was based on a mouse study, which used the HED of about 1.5g niacinamide daily. The mouse study actually saw reversal of pathology after 4 months of treatment. The human study used 3g daily AFAIK.
Nicotinamide Restores Cognition in Alzheimer's Disease Transgenic Mice via a Mechanism Involving Sirtuin Inhibition and Selective Reduction of Thr231-Phosphotau | Journal of Neuroscience

 

[haidut]

Y

Is a liquid glucose product coming ?

You mean dissolved in DMSO? There is probably no need. I may try a liquid ATP instead.

 

[johnwester130]

Y


You mean dissolved in DMSO? There is probably no need. I may try a liquid ATP instead.

what is liquid atp ?

 

[haidut]

what is liquid atp ?

ATP (the energy molecule) dissolved in something that can allow for transdermal absorption.

 

[WestCoaster]

Which is interesting, because Alzeimers for all intensive purposes can be called Type 3 diabetes, or insulin resistance in the brain. Insulin resistance as everyone should know is caused by excess glucose which your cells simply get sick of insulin knocking at the door to let glucose in. Alzeimers is an excess glucose problem which in turns leads to an insulin resistance problem in the brain which leads to glucose deprivation, which ultimately happens because the brain isn't trained to use the safer fuel (ketones) for energy.

To treat this is to simply do the opposite of what one did in the first place; get off glucose dependency, and train your body and brain to use ketones. Or to ensure one has minimal risk at developing alzeimers or some other brain disease in the first place, get off glucose dependency.

Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed
Neuroprotective and disease-modifying effects of the ketogenic diet

 

[Mary Pruter]

The human study was based on a mouse study, which used the HED of about 1.5g niacinamide daily. The mouse study actually saw reversal of pathology after 4 months of treatment. The human study used 3g daily AFAIK.
Nicotinamide Restores Cognition in Alzheimer's Disease Transgenic Mice via a Mechanism Involving Sirtuin Inhibition and Selective Reduction of Thr231-Phosphotau | Journal of Neuroscience

WoW. Thank you!

 

[ecstatichamster]

Which is interesting, because Alzeimers for all intensive purposes can be called Type 3 diabetes, or insulin resistance in the brain. Insulin resistance as everyone should know is caused by excess glucose which your cells simply get sick of insulin knocking at the door to let glucose in. Alzeimers is an excess glucose problem which in turns leads to an insulin resistance problem in the brain which leads to glucose deprivation, which ultimately happens because the brain isn't trained to use the safer fuel (ketones) for energy.

To treat this is to simply do the opposite of what one did in the first place; get off glucose dependency, and train your body and brain to use ketones. Or to ensure one has minimal risk at developing alzeimers or some other brain disease in the first place, get off glucose dependency.

Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed
Neuroprotective and disease-modifying effects of the ketogenic diet

Ray has said the opposite.

In the newsletter I just got, it contradicts what you are saying.

The brain consumes about 60% of the body's glucose when a person is physically inactive, and because of its dependence on glucose, it's easily damaged by even short periods of hypoglycemia. Most of its energy is used for a constant restructuring process-it never stops its developmental processes, though their intensity decreases with age. When hypoglycemia occurs during gestation or in infancy, when metabolic intensity is greatest, the adaptations can lead to life-long problem

and

Starvation and diabetes, in which glucose oxidation is limited, and amino acids and fatty acids are used for fuel, are pseudohypoxic states, forming lactic acid from both glucose and glutamine.

Hypoglycemia, besides causing unconsciousness and shock, can cause grand mal seizures, hypertension, vasospasm, and other excitatory processes, by leading to the release of glutamate and the activation o f the NMDA system.

This excitation creates reductive stress, resembling that in cancer cells, with the activation of the regulatory proteins, including HIF (the hypoxia inducible factor), that reinforce that state of inflammation and lactate produc- tion. Providing extra glucose can lower the HIF.

Of course the brain survives ketogenic diets. But does it do well on it?

 

[Mary Pruter]

I'm not sure if it was stated or not but my bottle of Niacinamide says that it should be taken on an empty stomach. The bottle of Tuerine says it also. Is this what you would recommend?

 

[Mary Pruter]

The exact directions say to take One A Day preferably between meals. Both my mother and I are doing 3 a day.

 

[haidut]

Ray has said the opposite.

In the newsletter I just got, it contradicts what you are saying.



and



Of course the brain survives ketogenic diets. But does it do well on it?

This news just in - the brain synthesizes its own fructose.
http://www.newsmax.com/Health/Health-News/brain-produce-sugar-obesity/2017/02/27/id/775741/
So, the whole premise of the ketogenic diet may be false - i.e. that the brain lives on ketones during ketosis. It is much more likely that the brain ramps up fructose synthesis in times of ketogenic stress and this is of course done by ramping up cortisol production.

 

[ecstatichamster]

Nice find, @haidut but, here is a better link:

JCI Insight - The human brain produces fructose from glucose

and

The press release from Yale:

 

[haidut]

Nice find, @haidut but, here is a better link:

JCI Insight - The human brain produces fructose from glucose

and

The press release from Yale:

Thanks, I just saw this today so did not have the time to dig around. Feel free to make a separate post about it if you want as it is an important corroboration of Peat's claims that the brain prefers glucose even when challenged by ketogenic diet.

 

[ecstatichamster]

the study says that the polyol pathway requires sugar...

The current data demonstrate that fructose is rapidly generated in the human brain during hyperglycemia.

the present observations suggest that endogenous human brain fructose production may be a key underappreciated factor modulating ingested sugar’s effect on the brain. While it is possible that plasma fructose may cross the BBB, we observed that the rise of intracerebral fructose occurred much earlier (by 20 minutes) than the modest increase in peripheral fructose levels (at 180 minutes).

However, fructose is almost never consumed in isolation, and our finding that glucose levels drive brain fructose levels suggests that any sugar consumption that raises circulating glucose may in large part mediate fructose’s effects in the brain. Why the human brain produces fructose at such high concentrations compared with the plasma remains unclear. In humans, Glut 5, the principal fructose transporter (33), is present predominantly on microglial cells (34, 35), raising the possibility that endogenous fructose production in the brain may alter neuronal and glial interactions.

A growing body of evidence suggests that chronic hyperglycemia leads to many adverse effects on brain function, particularly neurovascular disorders and cognitive impairment (36, 37). However, the underlying mechanisms behind these associations remain unclear. The current data demonstrating that fructose is produced in the human brain in response to hyperglycemia via the polyol pathway activity as well as evidence for the presence of aldose reductase, the rate-limiting enzyme in the polyol pathway, throughout the human brain, particularly in the cerebral cortex, basal ganglia, and hippocampus (11), may have particular implications for disordered eating behavior and disordered cognition in patients with diabetes.

 

[ecstatichamster]

The brain goes to great lengths to create fructose. Note this study was under hyperglycemic conditions. The test subjects (humans) were given 20% dextrose solution. The finding is that glucose turns into fructose in the brain, nothing to do with ketones if I'm understanding correctly.

 

[Regina]

The brain goes to great lengths to create fructose. Note this study was under hyperglycemic conditions. The test subjects (humans) were given 20% dextrose solution. The finding is that glucose turns into fructose in the brain, nothing to do with ketones if I'm understanding correctly.

I'm also confused by the "hyperglycemic" conditions.

 

[paymanz]

A growing body of evidence suggests that chronic hyperglycemia leads to many adverse effects on brain function, particularly neurovascular disorders and cognitive impairment

.

I'm not a expert but I wonder how they see it this way, the connection may be vice versa, the hyperglycemia itself may be a the product of the factors cause those disorders they mentioned.

Being inflammation or whatever that also causes inability to burn sugar...

 

[ecstatichamster]

I'm also confused by the "hyperglycemic" conditions.

the study shows the brain produces fructose from sugar. Even if no fructose sugar is given, the person's brain creates fructose in the brain it seems.