-S-
Nutrition Ketones as Treatment for Alzheimers? TedX Talk
- Thread starter Steve Freides
- Start date
- Status
-S-
Kenny Croxdale
Level 7 Valued Member
Ketones as Treatment for Alzheimers
This is a great presentation by Dr Mary Newport.Type III Diabetes
Alzheimers is now being labeled as Type III Diabetes.
One of the issues with Alzheimers is that the brain becomes unable to utilize glucose to essentially "Turn on the lights" and allow the brain to function.
The brain ends up starving because it is unable to utilize glucose to feed it.
Research shows, as Newport goes into, that the brain is able to utilize ketones to "Turn the lights on" and nourish it to some degree.
Thus, individuals with Alzheimers or cognitive disorders are able to function somewhat better.
Traumatic Brain Injury, TBI
Individuals who suffer from concussions also cannot utilize glucose effectively in the brain.
However, with TBI individuals are able to utilize ketones to run the brain.
"The Brain Is A Glucose Hog"
Normal individuals on a high carbohydrate diet require a lot of glucose to run the brain.
Research indicates that between 100-150 gram of glucose per day is needed for the brain to function.
However, all that changes when individuals...
Shifting To The Ketogenic Diet
Once "Keto Adapted" the brain primarily used ketones as fuel.
While the brain still needS some glucose. the amount of glucose needed on a Ketogenic Diet dropS down to 20%. 80% of the brains function driven by ketones.
That means rather than needing 100-150 gram of glucose per day, the brain works efficiently with around 20-30 gram a day.
That amount of glucose on a low carbohydrate diet is provide by the 50 gram or less of carbohydrates consumed, as well as...
Gluconeogenesis
This means the body breaks down some protein and triglycerides, converting them to glucose.
The Ketogenic Diet Is NOT Catabolic
Many individuals believe the Ketogenic Diet is catabolic, muscle being broken down into glucose; which isn't true on a well formulated Keto Diet.
Research shows that on a Keto Diet, ketones are preferred and the primary source of fuel; sparing glucose.
An indiviual who is "Keto Adapted '' is shown to have essentially the same amount of glucose as an individual on a high carbohydrate diet.
The caveat is that The Ketogenic Diet has converted the body's machinery to utilizing ketones, it is more effective at using ketone and does not access glycogen as efficiently.
Previous information on "How To Train On A Ketogenic Diet" has been posted on this site.
Secondly, the body becomes more efficient at utilizing ketone and sparing protein and muscle.
Research shows that Fasting up to 72 hours (Ketone State) primarily uses ketones, preserving muscle mass.
Third, research (Volek/Phinney) found higher Leucine levels in "Keto Adpated" individual. Leucine is the anabolic amino acid that maintains or increases muscle mass.
Preservation
The reason that the body primarily utilizes body fat (ketones), preserving muscle mass and increasing Leucine blood levels in Fasting or on a Ketogenic Diet is because the body autoregulates. It goes into survival mode.
It realizes that muscle mass is necessary for survival and body fat/ketones are expendable.
Add to that, let's say a 150 lb person is 15% body fat. That means they have 22.5 lb of body fat,
That mean they have 78,750 stored calories. (22.5 lbs body fat X 3500 calories per pound).
Now let's move to...
Feeding An Alzheimers Brain
These individuals need more ketones.
They can still consume a fairly high carbohydrate diet.
However, to obtain more ketones, they need to consume more fat...especially Coconut Oil and/or Medium Chain Trlglycridesm, MCT Oil.
As per Newport...
How Much Coconut Oil for Alzheimer's & Dementia?
1) Coconut Oil
2:50 minute mark
a) Ketone level peaks at about 3 hour after taking Coconut Oil.
b) Ketones remained in the system for 7 - 8 hours.
2) MCT Oil
3:00 minutes mark
a) Ketone level is higher but peaked at 90 minutes.
b) Ketones gone at 3 hours
Based on this information, it appears that a combination of Coconut Oil and MCT Oil would be most effective.
Coconut Oil provides a "Time Released" effect of ketones.
MCT Oil provides "Faster Released" ketones.
Metabolic Mitochondrial Damage
In 2016, I went on the Ketogenic Diet in conjunction with Intermittent Fasting after being diagnosed with this condition.
Research shows that with some forms of Metabolic Mitochondrial Damage, the Ketogenic Diet and Fasting helps.
However, this approach doesn't appear to work the same with my Metabolic Mitochondrial Damage condition.
However, the Ketogenic Diet and Fasting appears to work for me in a different way.
Epigenetics
What is Epigenetics? | CDC
Epigenetics is the study of how your behaviors and environment can cause changes that affect the way your genes work.
www.cdc.gov
Epigenetics is the study of how your behaviors and environment can cause changes that affect the way your genes work. Unlike genetic changes, epigenetic changes are reversible and do not change your DNA sequence, but they can change how your body reads a DNA sequence.
In plain English, diet can often change how your DNA is programmed in good or bad ways based on diet and some other external factor, outside the body.
DNA Sentence Example
1) We are hungry, let's eat grandma.
Sound like they are going to eat Grandma.
2) We are hungry. Let's eat, Grandma.
Sounds like they want Grandma to fix them something to eat.
Intermittent Fasting and The Ketogenic Diet
They are siblings. They promote some of the same health benefits.
Essentially, The Ketogenic Diet tricks the body into thinking it's to some degree in a Fasting State.
The Ketogenic Bible
This is one of the most in depth books on this (Drs Jacob Wilson and Ryan Lowery).
Part of it examines the benefits of The Ketogenic Diet for various diseases and disorders.
Take Home Message
1) Individuals with Cognitive Disorders usually improve when Coconut Oil or MCT Oil is added to their diet.
2) Strange but True...
Nicotine has been shown to improve Cognitive Brain Function.
NOT cigarettes but Nicotine Lozenges and Gum.
Last edited:
TimothyGander
Level 5 Valued Member
Do you have any ideas why the brain may not be able to process glucose? I usually encounter an opposite explanation - that due to oxidative damage to the mitochondria, the brain cannot utilize lipids, and thus has to rely on glucose for fuel, and this demand for glucose is a main driver of blood sugar increase.
Kenny Croxdale
Level 7 Valued Member
No Idea
I am no sure why the brain is unable to process and utilize glucose with Alzheimer's, Dementia, TBI (Traumatic Brain Injury), etc.
What research information do you have?
North Coast Miller
Level 9 Valued Member
A long read and deep dive, I've only scanned it once:
Reevaluating Metabolism in Alzheimer's Disease from the Perspective of the Astrocyte-Neuron Lactate Shuttle Model
The conventional view of central nervous system (CNS) metabolism is based on the assumption that glucose is the main fuel source for active neurons and is processed in an oxidative manner. However, since the early 1990s research has challenged the idea that the energy needs of nerve cells are...
"Moreover, recent evidence showed supplementation with the oxidative energy substrates pyruvate and 3-beta-hydroxybutyrate in vitro or in vivodecreased A-induced neuronal dysfunction supporting a protective role of active ETC in AD [98]. However, it is uncertain how these oxidative energy substrates restore neuronal function, and their effects on mitochondrial derived ROS in cell culture and animal models of AD remain unknown."
"Interestingly, in a recent study it was found that cancer survivors have a lower risk of developing AD than those without cancer [114]. In contrast, patients who suffered from AD had a lower risk of incident cancer [114]. It is possible that individuals with cancer also have a higher propensity to activate aerobic glycolysis, as this form of metabolism confers a growth and survival advantage (i.e., antiapoptotic function) to cancer cells [96]. However, individuals who survive cancer may still have higher innate levels of aerobic glycolysis, presumably in areas of the brain, which may protect against the development of AD. In contrast, patients with AD may have lower levels of aerobic glycolysis, which not only renders them susceptible to the toxic effects of A but also leads to decreased susceptibility to developing cancer. A similar trend has been observed in Parkinson’s disease [115, 116]."
Last edited:
- Status