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Old Age Dementia + C60oo

dementia c60oo

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#1 MacD

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Posted 27 July 2013 - 12:43 PM


I'm not going to write much here, except that my mother and I have taken the bold decision to give some c60oo to my Aunty who has severe dementia.

She is 92 years old and her short term memory is worse than that of a goldfish. She literally cant remember what she did 30 seconds ago.

First dose was today @ a 1.5mg dose.


Will report what happens.
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#2 niner

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Posted 27 July 2013 - 02:35 PM

Unlikely to hurt, and might indeed help. If the problem is transient ischemic attacks, then c60 may ameliorate damage, at least from future ischemia. Improved mitochondrial function should be beneficial regardless of the cause of the dementia. A search for alzheimers c60 turned up this report from Wired. It's about Andrievsky's hydrated fullerenes being tried against Alzheimer's. Here is the abstract of Podolski's work that the Wired post mentions. The mechanism by which amyloid beta causes neuronal cell death has been shown to involve a free radical process, so protection against radicals afforded by c60-oo should be helpful.

The ultimate result might be a slowing of your aunt's decline, or with luck, some improvement in her condition. Keep us posted.
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#3 AdamI

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Posted 27 July 2013 - 11:53 PM

PQQ do create more mitochondria. so that might be something as well. and curcumin that also have the capability to scavenge some beta amyloid. http://www.lef.org/m...with-PQQ_01.htm

#4 MacD

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Posted 28 July 2013 - 09:54 AM

First morning after first dose.

I asked my mother how my Aunty was and my mother said "just the same".

I am keeping a keen eye open though and i was able to have a conversation with my Aunty without her struggling to hear what i was saying.


Is it my wishful thinking, or is my Aunty more coherant?

#5 MacD

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Posted 28 July 2013 - 01:56 PM

This is no lie.

I have asked my Aunty today - "How do you feel", and she smiled at me and replied "My head feels a lot better today".


I see her everyday, and for the past year, her head has been causing her discomfort.


For the last 8 months, she barely knows where she is, neither does she recognise me and today she said "I am living in your mothers house, and you are my nephew".


This is no placebo effect on my part, this is a clear deviation from her previous normal behaviour.

Edited by MacD, 28 July 2013 - 01:57 PM.

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#6 markymark

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Posted 28 July 2013 - 05:42 PM

Elsewhere in this Forum I posted, that I gave one bottle (50 ml) to my old uncle (he is 90 years old), who has a myelodysplastic syndrome (low risk type) and just recovered from pneumonia and endocarditis. I decided to give him the C60-oo, because he escaped death only scantily and I am his Doctor as well.
This was in June. I will see him in the next weeks. On the phone, he made a very good impression to me while - and after taking the C60.

#7 MacD

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Posted 30 July 2013 - 08:08 PM

I wish well for your uncle Marky.


After one dose, my Aunty seemed a lot more coherant the next day, but alas, she has gone back to her old ways.

We will dose her with another 1.5mg on Saturday, and see how she is on Sunday.


If she shows another spurt of improvement, i will suggest to my mother we up the dose to 2-3 times per week and see what happens.

#8 AdamI

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Posted 31 July 2013 - 11:24 AM

I take 3 mg a day and I have been doing that since september, maybe you should increase it alot more... I'm 32 and healthy. Why these very smnall doses, isn't it better to just have a high dose at once so u can see the difference more clearly?
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#9 MacD

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Posted 31 July 2013 - 08:10 PM

I got home from work today, and she was particularly bad. She didn't know where she was or who i was.

I decided to give her a 2.25mg dose and left her for the evening.

When my mother got home, i asked her how Aunty was and my mother replied "better".

I then told her i had given her some more c60.


Going to up the dose to 3.0mg on Saturday and see how she is Sunday.


Is it coincidence that my Aunty had 2 better states of mentality after 2 doses of c60, or is the c60 actually doing something for her?

#10 Logic

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Posted 01 August 2013 - 09:59 AM

Perhaps have a look at Curcumin, EV Coconut Oil, B3, Methylene Blue too:

http://www.longecity...itive-enhancer/

http://www.longecity...from-the-brink/

EVCO should also help to minimise many of the low level chronic infections that old people suffer from due to the Lauric etc. acids in it.
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#11 mait

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Posted 01 August 2013 - 12:06 PM

Perhaps have a look at Curcumin, EV Coconut Oil, B3, Methylene Blue too:

http://www.longecity...itive-enhancer/

http://www.longecity...from-the-brink/

EVCO should also help to minimize many of the low level chronic infections that old people suffer from due to the Lauric etc. acids in it.


Plus EVCO helps in energy metabolism of the brain by providing ketone bodies that nerve cells can use as energy source. Alzheimer's disease has has insulin insensitivity as one of its symptoms, which has led some scientist to consider this disease as type III diabetes: http://www.ncbi.nlm....les/PMC2769828/

Alzheimer's disease (AD) has characteristic histopathological, molecular, and biochemical abnormalities, including cell loss; abundant neurofibrillary tangles; dystrophic neurites; amyloid precursor protein, amyloid-β (APP-Aβ) deposits; increased activation of prodeath genes and signaling pathways; impaired energy metabolism; mitochondrial dysfunction; chronic oxidative stress; and DNA damage. Gaining a better understanding of AD pathogenesis will require a framework that mechanistically interlinks all these phenomena. Currently, there is a rapid growth in the literature pointing toward insulin deficiency and insulin resistance as mediators of AD-type neurodegeneration, but this surge of new information is riddled with conflicting and unresolved concepts regarding the potential contributions of type 2 diabetes mellitus (T2DM), metabolic syndrome, and obesity to AD pathogenesis. Herein, we review the evidence that (1) T2DM causes brain insulin resistance, oxidative stress, and cognitive impairment, but its aggregate effects fall far short of mimicking AD; (2) extensive disturbances in brain insulin and insulin-like growth factor (IGF) signaling mechanisms represent early and progressive abnormalities and could account for the majority of molecular, biochemical, and histopathological lesions in AD; (3) experimental brain diabetes produced by intracerebral administration of streptozotocin shares many features with AD, including cognitive impairment and disturbances in acetylcholine homeostasis; and (4) experimental brain diabetes is treatable with insulin sensitizer agents, i.e., drugs currently used to treat T2DM. We conclude that the term “type 3 diabetes” accurately reflects the fact that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features that overlap with both type 1 diabetes mellitus and T2DM.



#12 MacD

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Posted 01 August 2013 - 03:35 PM

Thank you for these suggestions Logic.


They are something i will look in to.


For now, i have given my Aunty another 2.25mg of C60oo, she is definately "perky" a few hours after a dose and this seems to continue on to the next day. I want to stick with this for a while and see how her well-being develops.

#13 Logic

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Posted 01 August 2013 - 04:39 PM

Pleasure MacD. :)

It is interesting to see the results of the C60oo on your aunt here.
I think perhaps the duration of the positive effect will increase until her cells are well saturated with C60oo.
At this point it is probably prudent to stop giving it to her until her condition deteriorates once again.

By this point you should have had enough time to read through the pertinent information in the above links and be in a position to try B3 and Methylene Blue and EVCO.

You can find info on the B3 - Meth Blue combo in Turnbuckle's Profile page and here:
http://www.longecity...candida-and-b3/

Note that any Meth Blue stains are magically cleared up with an Ascorbic Acid/Vit C solution, and can be avoided by mixing it with Ascorbic Acid before dosing. ;)
Also Note that EVCO is very good at treating Candida.

#14 niner

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Posted 01 August 2013 - 11:16 PM

I think perhaps the duration of the positive effect will increase until her cells are well saturated with C60oo.
At this point it is probably prudent to stop giving it to her until her condition deteriorates once again.


Why is it prudent to stop until she deteriorates?
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#15 Logic

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Posted 02 August 2013 - 09:02 AM

Why is it prudent to stop until she deteriorates?

Well for the reasons you and Turnbuckle have discussed elsewhere in this forum Niner.Personally I like Turnbuckle's ...'natural selection' of the more healthy mitochondria reproducing and allowing the less healthy mitos to die off hypothesis, but I have not discounted your cancer concerns.Also it gives one a good idea of how long the effects of C60oo last in older people.The dosing schedule can then be adjusted accordingly so as to avoid deterioration.ie: If deterioration is noted 4 days after dosing; the schedule can be changed to a dose every 3 days?Perhaps PQQ on a schedule that fits in with these hypotheses should also be considered?

#16 Logic

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Posted 02 August 2013 - 10:52 AM

Oops: I have been having difficulty posting for a while now and have to toggle editing mode to OFF to post. It seems that all spacing has flown out the window too now. Soz

#17 Authentic

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Posted 24 August 2013 - 03:33 PM

MacD do you have any update? If so please post !

#18 MacD

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Posted 27 August 2013 - 09:35 AM

My Aunty has gotten a lot worse sadly.

She barely recognises anyone any doesn't know where she is.

I decided to stop the c60 dosing and let nature take it's course.

Sorry, but I dont have much more to report than that. Perhaps if she had started c60 years earlier, it may have been a preventative measure. Perhaps not, I don't know.

#19 mait

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Posted 27 August 2013 - 01:30 PM

My Aunty has gotten a lot worse sadly.

She barely recognises anyone any doesn't know where she is.

I decided to stop the c60 dosing and let nature take it's course.

Sorry, but I dont have much more to report than that. Perhaps if she had started c60 years earlier, it may have been a preventative measure. Perhaps not, I don't know.


It is very sad news to hear. I wish You and Your family all the best.
At what time did You drop the c60 doing (recently or for a while ago) and what was the dosage at the time, when You stopped the C60 dosing?

#20 hav

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Posted 27 August 2013 - 06:48 PM

My Aunty has gotten a lot worse sadly.

She barely recognises anyone any doesn't know where she is.

I decided to stop the c60 dosing and let nature take it's course.

Sorry, but I dont have much more to report than that. Perhaps if she had started c60 years earlier, it may have been a preventative measure. Perhaps not, I don't know.


It's such a tough and heart wrenching circumstance. My heart goes out to both of you.

My mom was 87 last year when she passed after a period of dementia so I know how it is. It was tough letting nature take its course but that's the way she wanted it. My dad's 96 and still sharp as a tack but not interested in anything adulterating his beloved olive oil which he's been big on his whole life. Each to their own elixir.

Howard

#21 Turnbuckle

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Posted 27 August 2013 - 07:22 PM

For others thinking of trying C60 for AZ, I suggest you look at this article--


Memory loss is the signature feature of Alzheimer's disease, and therapies that prevent or delay its onset are urgently needed. Effective preventive strategies likely offer the greatest and most widespread benefits. Histone deacetylase (HDAC) inhibitors increase histone acetylation and enhance memory and synaptic plasticity. We evaluated the efficacy of nicotinamide, a competitive inhibitor of the sirtuins or class III NAD(+)-dependent HDACs in 3xTg-AD mice, and found that it restored cognitive deficits associated with pathology. Nicotinamide selectively reduces a specific phospho-species of tau (Thr231) that is associated with microtubule depolymerization, in a manner similar to inhibition of SirT1. Nicotinamide also dramatically increased acetylated alpha-tubulin, a primary substrate of SirT2, and MAP2c, both of which are linked to increased microtubule stability. Reduced phosphoThr231-tau was related to a reduction of monoubiquitin-conjugated tau, suggesting that this posttranslationally modified form of tau may be rapidly degraded. Overexpression of a Thr231-phospho-mimic tau in vitro increased clearance and decreased accumulation of tau compared with wild-type tau. These preclinical findings suggest that oral nicotinamide may represent a safe treatment for AD and other tauopathies, and that phosphorylation of tau at Thr231 may regulate tau stability.


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#22 Authentic

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Posted 27 August 2013 - 07:29 PM

Turnbuckle have you found any updates on the clinical trial for nicotinamide? I can find the trial but no results.

http://www.life-enha...heimers-neurons

http://clinicaltrial...how/NCT00580931

#23 Turnbuckle

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Posted 27 August 2013 - 07:49 PM

Turnbuckle have you found any updates on the clinical trial for nicotinamide? I can find the trial but no results.

http://www.life-enha...heimers-neurons

http://clinicaltrial...how/NCT00580931


No. But there was a retrospective study that found an advantage for dietary niacin, even small amounts--

http://www.ncbi.nlm..../v075p01093.pdf

From that paper--

Attached Files



#24 Logic

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Posted 28 August 2013 - 12:48 PM

For others thinking of trying C60 for AZ, I suggest you look at this article--


Memory loss is the signature feature of Alzheimer's disease, and therapies that prevent or delay its onset are urgently needed. Effective preventive strategies likely offer the greatest and most widespread benefits. Histone deacetylase (HDAC) inhibitors increase histone acetylation and enhance memory and synaptic plasticity. We evaluated the efficacy of nicotinamide, a competitive inhibitor of the sirtuins or class III NAD(+)-dependent HDACs in 3xTg-AD mice, and found that it restored cognitive deficits associated with pathology. Nicotinamide selectively reduces a specific phospho-species of tau (Thr231) that is associated with microtubule depolymerization, in a manner similar to inhibition of SirT1. Nicotinamide also dramatically increased acetylated alpha-tubulin, a primary substrate of SirT2, and MAP2c, both of which are linked to increased microtubule stability. Reduced phosphoThr231-tau was related to a reduction of monoubiquitin-conjugated tau, suggesting that this posttranslationally modified form of tau may be rapidly degraded. Overexpression of a Thr231-phospho-mimic tau in vitro increased clearance and decreased accumulation of tau compared with wild-type tau. These preclinical findings suggest that oral nicotinamide may represent a safe treatment for AD and other tauopathies, and that phosphorylation of tau at Thr231 may regulate tau stability.


Yep; see post #13
http://www.longecity...post__p__602683
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#25 Turnbuckle

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Posted 28 August 2013 - 06:53 PM

Note that any Meth Blue stains are magically cleared up with an Ascorbic Acid/Vit C solution, and can be avoided by mixing it with Ascorbic Acid before dosing.


Now that is interesting! But mixing it with C beforehand doesn't destroy its activity?

#26 niner

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Posted 28 August 2013 - 08:29 PM

Note that any Meth Blue stains are magically cleared up with an Ascorbic Acid/Vit C solution, and can be avoided by mixing it with Ascorbic Acid before dosing.


Now that is interesting! But mixing it with C beforehand doesn't destroy its activity?


Nope, not only does C not hurt MB, it actually makes it better. The new (colorless) compound is just the reduced form of MB, known as leucomethylene blue. TauRx, the company that was bringing MB to market as an AD treatment under the name "Rember" have modified their application. They've gone back and run at least one trial using LMB. They found that they could get by with a somewhat lower dose. It's still in mid double digit milligram range. LMB is also a lot easier for patients to tolerate, compared to MB. It's also being trialed in frontotemporal dementia, which is a pretty big deal since there aren't any great agents for that. MB/LMB looks to be useful in other neurodegenerative conditions as well. I suspect that making mitochondria work better is a good thing for these conditions in general. The dosage they're using with Rember is similar to the level that Atamna used in his mitochondial function paper.

#27 Turnbuckle

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Posted 28 August 2013 - 08:42 PM

Tried it and the color is (almost) gone. So now if I take a substantial amount of this, will it stay reduced--ie, colorless?

#28 BioFreak

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Posted 11 November 2013 - 05:57 PM

I STRONGLY suggest longvida curcumin. My grandma (101) with dementia does take it, and it makes a world of a difference, even only at 1000mg. We never tried 2000mg because it is so expensive. Expensive, because we use longvida curcumin which is the ONLY curcumin formula which is proven to cross the bbb in studies. Meriva, sabinsa, bcm-95, forget em. Sabinsa c3 complex can work for non-brain issues, but only if you dose it high(i.e. 8g) and use piperine, maybe quercerin, additional oil, to improve its bioavailability, and take it all at ONCE each day, no split dosages. Theracurmin looks promising but no proof studies that it does cross the bbb yet. There is a world of a difference between the different kinds of curcumin formulations. Oh yea, and there is not much use beyond 2g longvida curcumin/day, because blood levels do not rise much more with higher dosages.

So that are the most important infos when it comes to curcumin, in a nutshell.

My grandma shows with longvida curcumin:
  • a higher stress threshold,
  • better short term memory,
  • a bit less anxiety,
  • more reasoning / IQ then in her normal dementia state,
  • less / no hallucinations (depending on stress also),
  • better spacial / temporal orientation
  • she does not call for me every 2 minutes
  • and she is more reasonable.
  • In short her brain simply works better... it's an remarkable difference and makes care taking so much easier.
  • And it eases pain though its antiinflammatory action (you could, however use another brand for that, but you'd need for example 8g of sabinsa c3 complex to get the same blood levels as with longvida)
  • And it removes amyloid since it can cross the bbb, which starts to form as soon as in the 30ties in 90% of humans.
So let me tell you as someone who does take care of his grandma every day for 10 months now, GET THAT LONGVIDA CURCUMIN.
Effects can be seen as soon as 1-2 days after dosing, and even after weeks we saw more improvements.

My grandma never tried c60 because it would be cruel to make her live even longer with all the health problems she has that can not be cured by c60(horrible bone deformations due to osteoporosis for example, almost blind and deaf).

#29 Authentic

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Posted 11 November 2013 - 07:40 PM

I'm thinking to try the LEF Super Bio-curcumin, 400mg instead. it's a lot less expensive.

#30 niner

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Posted 11 November 2013 - 08:19 PM

My grandma never tried c60 because it would be cruel to make her live even longer with all the health problems she has that can not be cured by c60(horrible bone deformations due to osteoporosis for example, almost blind and deaf).


Thanks for the Longvida tip. I might try that with my mother in law at some point. Regarding not using c60 in an elderly person, I wouldn't worry about making them suffer longer. For one thing, starting that late in life, the damage is already done, and I don't think that c60 will result in a substantial life extension. On the other hand, it might provide a much improved quality of life while she is still alive. The logic that you're applying here could be applied to any medication that might prevent death, although I presume she already has a "Do Not Resuscitate" order. (If not, perhaps it would be a consideration.) This is a thorny moral/emotional issue. It's not simple at all, but I have to wonder where something like a DNR order or withholding medication ends, and euthanasia begins, or why it shouldn't. Sorry, these ramblings probably aren't making anything easier. It's a hard problem. I hope she's comfortable, and I'm glad the Longvida is working out.




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