Vince
Super Moderator
I would add MCT oil and fish oil to your wife's diet. Medium and long chain fat may help with her dementia.
Dementia - Alzheimer's
- Thread starter Vince
- Start date
Thank you, Vince. I watched a TED talk by a physician whose husband has dementia and that was the topic of her talk. My wife, though, is resistant to anything outside her comfort zone. My primary, who is also a caregiver, counseled me that if someone is resistant, there's nothing that can be done. She seems not to have the will to survive, though she knows from watching her sisters succumb to dementia, what the future holds. I can't understand someone who refuses to try and that leaves me frustrated, angry and sad.
As I've written on other posts, we've not had a good marriage but she's still someone I've spent 30 years with( good times, bad times) and to watch her decline; to see the end play out in slow motion, is devastating.
Vince
Super Moderator
Have you read about melatonin and people with dementia. They need to reset their sleep clock daily by taking 10 mg of melatonin broken down in water and take. Half hour before sunset and 2 hours before bed.
Vince
Super Moderator
Sundowning.
www.ncbi.nlm.nih.gov
Clinical Aspects of Melatonin Intervention in Alzheimer’s Disease Progression - PMC
Melatonin secretion decreases in Alzheimer´s disease (AD) and this decrease has been postulated as responsible for the circadian disorganization, decrease in sleep efficiency and impaired cognitive function seen in those patients. Half of severely ...
www.ncbi.nlm.nih.gov
Vince, I do appreciate your sharing what you know. Again, she's not into trying anything, whether dietary changes or supplements. Maybe with a better,knowledgeable doctor, she'd be amenable but not with me. And, if she took something at my suggestion and she had a bad reaction to it, that would be the end of that. My mother was like that as my father and I tried dietary approaches and supplements for her metastatic colon cancer, since there weren't effective treatments back in the 70's. She resisted, though she was in pain and didn't want to die.
Thank you. I read the link. The one significant side effect that I experienced as did a friend is diahrrea...severe. My friend had it for several weeks and was admitted to the hospital. I told her about this side effect. She stopped the drug and it cleared up.
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What was the total daily dose at which diarrhea appeared? Gabapentin is used as a sleep aid at night and at low doses, that are in the range of the second study 100-600mg daily. I doubt it needs to be taken at huge doses during the day at all. It boosts production of GABA in the brain which is a long post drug effect, not an acute effect when the drug is taken.
Kenny Croxdale
New 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.
Kenny Croxdale
New Member
Individual Who Don't Care
As your primary stated, there nothing you can do for someone who is resistant and doesn't care.
My Sister
My sister has been pre-diabetic for about 10 years. I've tried talking to her about modifying her diet; which is high in junk food.
It's too much work for her. She'd rather pop pills than change her diet. However, popping pills hasn't worked.
My brother-in-law is diabetic. He continues to eat junk food. To combat that, he just increases his insulin dosage, then eat more candy bars.
The Take Home Message
Unfortunately, you cannot help someone who does't want to be help.
Like your wife, the fact that my sister could do something but doesn't care enough to do so, continues to bother me.
There nothing you can do until someone want to make the effort. It's a waste of time. All it does create problem for them and you, as I found out with my sister.
Might as well reiterate this list of medications and supplements:
Huperzine A—“For some years, huperzine A has been investigated as a possible treatment for diseases characterized by neurodegeneration, particularly Alzheimer's disease.[2][13] A 2013 meta-analysis found that huperzine A may be efficacious in improving cognitive function, global clinical status, and activities of daily living for individuals with Alzheimer's disease. However, due to the poor size and quality of the clinical trials reviewed, huperzine A should not be recommended as a treatment for Alzheimer's disease unless further high quality studies confirm its beneficial effects.[4]”
Alpha glycerylphosphorylcholine (GPC)—“… a natural choline compound found in the brain. It is also a parasympathomimetic acetylcholine precursor which has been investigated for its potential for the treatment of Alzheimer's disease and other dementias.”
Phosphatidylserine—“A 2020 meta-analysis of relevant clinical trials found that phosphatidylserine is likely effective for enhancing cognitive function in older people with mild cognitive impairment.”
Selegiline—“The monoamine oxidase-B inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson’s disease and possibly Alzheimer’s disease. The neuroprotective property of L-deprenyl may be unrelated to the inhibition of monoamine oxidase-B. Since nitric oxide (NO) modulates activities including cerebral blood flow and memory, we examined the effect of L-deprenyl on NO. L-Deprenyl induced rapid increases in NO production in brain tissue and cerebral vessels. Vasodilation was produced by endothelial NO- dependent as well as NO-independent mechanisms in cerebral vessels. The drug also protected the vascular endothelium from the toxic effects of amyloid-beta peptide. These novel actions of selegiline may protect neurons from ischemic or oxidative damage and suggest new therapeutic applications for L- deprenyl in vascular and neurodegenerative diseases.”
PDE5 inhibitor—“Specifically, various rodent studies have reported that PDE5 inhibitors can reverse cognitive impairments and pathology in aged wild-type mice and transgenic Alzheimer’s mouse models through mechanisms including reduced tau hyperphosphorylation (via GSK3β activation), increased BDNF, anti- inflammatory action, increased pCREB signaling, and reduced apoptosis and cell death [2; 3; 4; 5]. Beta- amyloid pathology has been reversed in some [3; 6] but not all [2; 5] studies.
“Whether these effects will occur in humans has yet to be tested. No human studies, observational or randomized, have examined if the use of PDE5 inhibitors can protect against dementia or brain aging.”
Lithium—“One study found that long-term lithium exposure from drinking water may be associated with a lower risk of being diagnosed with dementia. … One epidemiological study in Texas revealed that rates of death from Alzheimer’s were higher in areas with low levels of lithium in the water. In one clinical study, a micro-dose of just 300 mcg of lithium daily was found to significantly decrease cognitive decline in Alzheimer’s patients, compared to a placebo.”
www.lifeextension.com
Palmitoylethanolamide—(One of two PEAs) “Either preclinical or clinical studies indicate that PEA is potentially useful in a wide range of therapeutic areas, including eczema, pain, and neurodegeneration. … In the present review, we summarized the current preclinical and clinical evidence of PEA as a possible therapeutic agent in Alzheimer's disease. The possible PEA neuroprotective mechanism(s) of action is also described.”
pubmed.ncbi.nlm.nih.gov
"Palmitoylethanolamide protects against the amyloid-β25-35-induced learning and memory impairment in mice, an experimental model of Alzheimer disease"
www.ncbi.nlm.nih.gov
Vascular dementia and aliamides: A new approach for the future
www.oatext.com
DHEA
Pregnenolone
“Pregnenolone sulfate and DHEA sulfate have also been found to improve cognition in animal studies[111][112][113][114][115][116][117][118]. In an animal model of b amyloid-induced amnesia, DHEA, DHEA sulfate, and pregnenolone sulfate attenuated amnesia in a dose-dependent manner[119]. Interestingly, inhibition of the steroid sulfatase enzyme improved the antiamnesic effect of DHEA sulfate[120][121], indicating that preventing neuroactive steroids from being converted out of their sulfate form may improve cognition.
“Nevertheless, the non-sulfated form of pregnenolone has been shown to improve cognition[122][123] and function[124][125] in schizophrenics. Schizophrenia is characterized by elevations in DHEA and DHEA sulfate and decreases in allopregnanolone, though it is yet unknown how pregnenolone is exerting its effect[126]. It was observed that changes in plasma steroid levels of pregnenolone and allopregnanolone correlated with functional improvements. Interestingly, studies indicate pregnenolone produces biphasic results, where lower dosed (30 mg/day) treatments produced better outcomes than higher dosed treatments (200 mg/day).”
www.leoandlongevity.com
Huperzine A—“For some years, huperzine A has been investigated as a possible treatment for diseases characterized by neurodegeneration, particularly Alzheimer's disease.[2][13] A 2013 meta-analysis found that huperzine A may be efficacious in improving cognitive function, global clinical status, and activities of daily living for individuals with Alzheimer's disease. However, due to the poor size and quality of the clinical trials reviewed, huperzine A should not be recommended as a treatment for Alzheimer's disease unless further high quality studies confirm its beneficial effects.[4]”
Alpha glycerylphosphorylcholine (GPC)—“… a natural choline compound found in the brain. It is also a parasympathomimetic acetylcholine precursor which has been investigated for its potential for the treatment of Alzheimer's disease and other dementias.”
Alpha-GPC
L-Alpha glycerylphosphorylcholine (alpha-GPC, choline alfoscerate) is a natural choline compound found in the brain. It is also a parasympathomimetic acetylcholine precursor which has been investigated for its potential for the treatment of Alzheimer's disease and other dementias. Alpha-GPC...
dbpedia.org
Phosphatidylserine—“A 2020 meta-analysis of relevant clinical trials found that phosphatidylserine is likely effective for enhancing cognitive function in older people with mild cognitive impairment.”
Selegiline—“The monoamine oxidase-B inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson’s disease and possibly Alzheimer’s disease. The neuroprotective property of L-deprenyl may be unrelated to the inhibition of monoamine oxidase-B. Since nitric oxide (NO) modulates activities including cerebral blood flow and memory, we examined the effect of L-deprenyl on NO. L-Deprenyl induced rapid increases in NO production in brain tissue and cerebral vessels. Vasodilation was produced by endothelial NO- dependent as well as NO-independent mechanisms in cerebral vessels. The drug also protected the vascular endothelium from the toxic effects of amyloid-beta peptide. These novel actions of selegiline may protect neurons from ischemic or oxidative damage and suggest new therapeutic applications for L- deprenyl in vascular and neurodegenerative diseases.”
PDE5 inhibitor—“Specifically, various rodent studies have reported that PDE5 inhibitors can reverse cognitive impairments and pathology in aged wild-type mice and transgenic Alzheimer’s mouse models through mechanisms including reduced tau hyperphosphorylation (via GSK3β activation), increased BDNF, anti- inflammatory action, increased pCREB signaling, and reduced apoptosis and cell death [2; 3; 4; 5]. Beta- amyloid pathology has been reversed in some [3; 6] but not all [2; 5] studies.
“Whether these effects will occur in humans has yet to be tested. No human studies, observational or randomized, have examined if the use of PDE5 inhibitors can protect against dementia or brain aging.”
Lithium—“One study found that long-term lithium exposure from drinking water may be associated with a lower risk of being diagnosed with dementia. … One epidemiological study in Texas revealed that rates of death from Alzheimer’s were higher in areas with low levels of lithium in the water. In one clinical study, a micro-dose of just 300 mcg of lithium daily was found to significantly decrease cognitive decline in Alzheimer’s patients, compared to a placebo.”
How Does Lithium Work In The Brain? - Life Extension
Lithium may slow degenerative processes by inhibiting an age-accelerating enzyme in the brain and other organs.
Palmitoylethanolamide—(One of two PEAs) “Either preclinical or clinical studies indicate that PEA is potentially useful in a wide range of therapeutic areas, including eczema, pain, and neurodegeneration. … In the present review, we summarized the current preclinical and clinical evidence of PEA as a possible therapeutic agent in Alzheimer's disease. The possible PEA neuroprotective mechanism(s) of action is also described.”
Palmitoylethanolamide (PEA) as a Potential Therapeutic Agent in Alzheimer's Disease - PubMed
<span><i>N</i>-Palmitoylethanolamide (PEA) is a non-endocannabinoid lipid mediator belonging to the class of the <i>N</i>-acylethanolamine phospolipids and was firstly isolated from soy lecithin, egg yolk, and peanut meal. Either preclinical or clinical studies indicate that PEA is potentially...
pubmed.ncbi.nlm.nih.gov
Palmitoylethanolamide Protects Against the Amyloid-β25-35-Induced Learning and Memory Impairment in Mice, an Experimental Model of Alzheimer Disease - PMC
Alzheimer disease (AD) is the most common form of neurodegenerative dementia. Amyloid-β deposition, neurofibrillary tangle formation, and neuro-inflammation are the major pathogenic mechanisms that in concert lead to memory dysfunction and decline ...
www.ncbi.nlm.nih.gov
Vascular dementia and aliamides: A new approach for the future
OA Text is an independent open-access scientific publisher showcases innovative research and ideas aimed at improving health by linking research and practice to the benefit of society.
www.oatext.com
DHEA
Pregnenolone
“Pregnenolone sulfate and DHEA sulfate have also been found to improve cognition in animal studies[111][112][113][114][115][116][117][118]. In an animal model of b amyloid-induced amnesia, DHEA, DHEA sulfate, and pregnenolone sulfate attenuated amnesia in a dose-dependent manner[119]. Interestingly, inhibition of the steroid sulfatase enzyme improved the antiamnesic effect of DHEA sulfate[120][121], indicating that preventing neuroactive steroids from being converted out of their sulfate form may improve cognition.
“Nevertheless, the non-sulfated form of pregnenolone has been shown to improve cognition[122][123] and function[124][125] in schizophrenics. Schizophrenia is characterized by elevations in DHEA and DHEA sulfate and decreases in allopregnanolone, though it is yet unknown how pregnenolone is exerting its effect[126]. It was observed that changes in plasma steroid levels of pregnenolone and allopregnanolone correlated with functional improvements. Interestingly, studies indicate pregnenolone produces biphasic results, where lower dosed (30 mg/day) treatments produced better outcomes than higher dosed treatments (200 mg/day).”
The Power of Neuroactive Steroids
This article introduces the reader to the biosynthesis of neuroactive hormones and reviews what we know about their effects on cognition.
www.leoandlongevity.com
Vince
Super Moderator
Thankfully I'm apo-e 3/3
A variant of the so-called Alzheimer's gene, APOE4, seems to interfere with brain cells' ability to use insulin, which may eventually cause the cells to starve and die. Unofficially, it's called Type 3 diabetes. "What it refers [to] is that their brain's insulin utilization or signaling is not functioning.Nov 7, 2017
Mayo Clinic News Network › ...
A variant of the so-called Alzheimer's gene, APOE4, seems to interfere with brain cells' ability to use insulin, which may eventually cause the cells to starve and die. Unofficially, it's called Type 3 diabetes. "What it refers [to] is that their brain's insulin utilization or signaling is not functioning.Nov 7, 2017
Mayo Clinic News Network › ...
Mayo Clinic Minute: Is Alzheimer's Type 3 diabetes?
That's it.
Kenny, you, Cataceous and Vince all provide good and compelling information but as you wrote, "Unfortunately, you cannot help someone who doesn't want to be helped." At the moment, that's what I'm dealing with. Perhaps, if my wife had a knowledgeable doctor, whether a primary or neurologist, that person could make the case for her to change her diet and add specific supplements. And that's MAYBE. As it stands, all I can do is watch her slowly die.
We might be moving back to Maryland, near DC, where she has family and where she can get better medical care. She's even resistant to moving back after telling me, endlessly, how she misses her sister, who's now in memory care with advanced dementia. My wife's primary is mediocre and only knows how to write prescriptions. The neurologist is equally second rate. Keep pushing the boulder up the hill.
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Vince
Super Moderator
Wonder if you could get her in National Institutes of Health (NIH) it's in Maryland. I have been there with my first wife.
My wife worked there for 42 years, working her way up from clerical to assistant to the director of the Clinical Center. I was in-patient psychiatric in 1991. We met a few months before my discharge. It's a possibility. She has mixed feelings about leaving Florida, though she at first didn't want to live here. Her nieces are encouraging her(us) to move back.
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