Give her some blueberries when you can, and blueberry jam as a breadspread.
Sugar-free blueberry jams are in the market, but can taste a bit sour and acid.
The French "St Dalfour" brand has the highest fruit content at 55 per cent.
I've bought mum fresh blueberries in the past, but a lot of them got wasted due to carers ignoring foods in the fridge that were clearly marked with her name.
I don't want mum to eat jam on bread as this sticks to teeth. Night staff aren't very efficient when it comes to cleaning mum's teeth in the morning and I don't want her to get tooth decay or gum disease. 55% fruit content is still 45% added sugar.
I'd rather get mum turmeric tablets, as my previous link referred to bisdemethoxycurcumin receptors in the brain. Unfortunately, turmeric tablets are unchewable. As mum tries to chew everything that goes in her mouth, she'll spit them out (been there, done that).
There's another sugar-free brand here, Steffi's Delight, German-made.
Not sure if you have it there. Comes in a small 225 gram jar.
As for those jams with sugar, the balance of the jam is not all sugar,
of course. Mostly pectin or agar, with about 20-30 per cent added sugar,
typically making a total of 60 per cent sugar. The other 30-40 per cent
is inherent in the fruit itself.
Here's another sugar-free jam with a far better jar, not sure of the fruit
content though.
Seems it is carbohydrate-free too ? How did they manage
to make it that way ?
" Serrapeptase doesn’t just dissolve this precursor of silk, it can dissolve a
number of different proteins in the human body, including amyloid plaque .... "
" Serrapeptase doesn't just dissolve this precursor of silk, it can dissolve a number of different proteins in the human body, including amyloid plaque .... "
I don't think that the serrapeptidase could get access to the amyloid plaque. It would have to get past the stomach (acid and proteases), then get past the BBB, then get into the plaque locations. The combined odds of all this seem very low to me.
I don't think that the serrapeptidase could get access to the amyloid plaque. It would have to get past the stomach (acid and proteases), then get past the BBB, then get into the plaque locations. The combined odds of all this seem very low to me.
Anecdotal reports, but serrapeptase has a very impressive reputation on the net.
This person asked the same question about the chances of it crossing the blood-brain barrier, though.
" I used Serrapeptase to dissolve the protective protein coating around a lung cancer several years ago. Then my immune system was able to completely destroy the cancer as proven by x-ray evidence. "
" I started taking 9 capsules a day in divided doses and the tumor dissolved painlessly and inexpensively within 6 weeks. My doctor was flabbergasted when he saw the absolutely clean chest x-rays. "
" As I was taking Serrapeptase for some cysts at the time, I increased the dose to 160 000 units, hoping it would dissolve the floater. To my amazement, within two weeks after the accident the floater paled into a completely transparent, almost invisible structure. "
NT-020, comprising lowbush blueberry, carnosine, EGCG, D3 and grape seed extract,
formulation developed by South Florida university researchers, claimed to enhance
stem cell formation.
Restoring Memory, Repairing Damaged Brains With An Artificial Hippocampus.
“No hippocampus,” says Berger, “no long-term memory, but still short-term memory.”
CA3 and CA1 interact to create long-term memory, prior research has shown.
" These results demonstrate dim light at night is sufficient to reduce synaptic spine
connections to CA1. Importantly, the present results suggest that night-time low
level illumination, comparable to levels that are pervasive in North America and
Europe, may contribute to the increasing prevalence of mood disorders. "
Since CA1/CA3 signalling in the hippocampus is responsible for the conversion
of short to long term memories and is one of the first regions to be hit in
Alzheimer's, I would presume that artificial night lighting is a crucial factor in
the increasing incidence of this disease..
" A reduction in cerebral glucose utilization is one of the earliest signs of Alzheimer's disease. Although the exact cause of this reduction is not known, gathering evidence suggests that it is part of a complex metabolic adaptation to oxidative stress during which glycolysis and oxidative phosphorylation are turned down, glucose metabolism is shifted to the pentose phosphate pathway to generate antioxidant reducing factors such as nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione, and the gamma-aminobutyric acid (GABA) shunt is activated to provide glutamate as an alternate source of energy.
In the face of these adaptive metabolic changes, the Alzheimer brain runs short of energy and begins to digest itself.
Evidence is presented that gammahydroxybutyrate, a natural product of the GABA shunt, can provide the necessary energy, carbon, and antioxidant power and that its use may be able to delay the onset and progress of Alzheimer's disease. "
Alzheimer' s disease, oxidative stress and gammahydroxybutyrate.
" A reduction in cerebral glucose utilization is one of the earliest signs of Alzheimer's disease. Although the exact cause of this reduction is not known, gathering evidence suggests that it is part of a complex metabolic adaptation to oxidative stress during which glycolysis and oxidative phosphorylation are turned down, glucose metabolism is shifted to the pentose phosphate pathway to generate antioxidant reducing factors such as nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione, and the gamma-aminobutyric acid (GABA) shunt is activated to provide glutamate as an alternate source of energy.
In the face of these adaptive metabolic changes, the Alzheimer brain runs short of energy and begins to digest itself.
Evidence is presented that gammahydroxybutyrate, a natural product of the GABA shunt, can provide the necessary energy, carbon, and antioxidant power and that its use may be able to delay the onset and progress of Alzheimer's disease. "
A reduction in cerebral glucose utilization is one of the earliest signs of Alzheimer's disease (...) glucose metabolism is shifted to the pentose phosphate pathway (...) the Alzheimer brain runs short of energy and begins to digest itself
wow I'm not a specialist on AD but doesn't it seem like key to understand the biology of the disease?!? Do you know if mice engineered to repeatedly use pentose rather than glucose (eg when fed a drug) have AD-like signs?
I think the key to treating Alzheimer's disease is clearing out the junk (A-beta, tau tangles, what-not) in combination with drugs/substances that promote neuron growth - like perhaps this one that works wonders - in mice, anyways.
“This is about recovering function,” he says. “That’s what makes these things totally unique. They’re not designed necessarily to stop anything. They’re designed to fix what’s broken. As far as we can see, they work.” Harding, College of Arts and Sciences Professor Jay Wright and other WSU colleagues report their findings in the online “Fast Forward” section of the Journal of Pharmacology and Experimental Therapeutics. Their drug comes as the pharmacological industry is struggling to find an effective Alzheimer’s treatment. Last month, the Pharmaceutical Research and Manufacturers of America, or PhRMA, reported that only three of 104 possible treatments have been approved in the past 13 years. “This 34 to one ratio of setbacks to successes underlines the difficulty of developing new medicines for Alzheimer’s,” the trade group said in a news release. Development of the WSU drug is only starting. Harding and Wright must first satisfy the U.S. Food and Drug Administration that it is safe. Only then would clinical trials begin to see if a drug that works in a rat will work in a human. Safety testing alone could cost more than $1 million, says Harding, who is looking to fund the drug’s development through his and Wright’s company, M3 Biotechnology Inc., the WSU Research Foundation, and ultimately large pharmaceutical company partners. Harding, a medicinal chemist, and Wright, a neuroscientist, have been working on their compound since 1992, when they started looking at the impact of the peptide angiotensin IV on the hippocampus, a brain region involved in spatial learning and short-term memory. Typically, angiotensins have been linked to blood pressure regulation, but Harding and Wright noticed that angiotensin IV, or early drug candidates based on it, were capable of reversing learning deficits seen in many models of dementia.
I am a bit disturbed by many of the "failures" reported through the years in regards to targetting A-beta, and I think the term "failure" is rooted in the fact that aging is not considered a disease. There are many drugs/methods available now that can clear A-beta, but they are considered "failures" because the patients did not significantly recover past mental functionality after treatment. These treatments are not a "failure" IMO. They worked. They cleared junk out of the brain. Now those brains just need to be stimulated again and be given treatments to regrow neurons that were lost through decades of aging.
Anecdotal report of the common homeopathic remedy, Arnica, taken at 1M potency.
MENTAL DEGENERATION IN THE AGED 1M
" I used Arnica 1M dose 1 tsp daily in the case of a 75 year old who was showing signs of Alzheimer's and he showed perceptible improvement in 2 weeks which was continued thereafter. He is now permanently on the Arnica. Dose 1 tsp daily. "
" Brains of AD patients undergo many changes, such as disruption of protein
synthesis and degradation, classically associated with the heat shock response,
which is one form of stress response. "
" In particular, curcumin, a powerful antioxidant derived from the curry spice turmeric,
has emerged as a strong inducer of the heat shock response. In light of this finding,
curcumin supplementation has been recently considered as an alternative, nutritional
approach to reduce oxidative damage and amyloid pathology associated with AD. "
Metabolite Profiling of Alzheimer's Disease Cerebrospinal Fluid.
" Increased cortisol levels seemed to be related to the progression of AD and have been detected in more severe forms of AD. Increased cysteine associated with decreased uridine was the best paired combination to identify light AD with specificity and sensitivity above 75%. "
Note that the study is on Cordyceps ophioglossoides, rather than Cordyceps sinensis, the Chinese cordyceps commonly sold as an adaptogen and supplement.
Cordyceps ophioglossoides is widely distributed in eastern North America.
Mycelial extract of Cordyceps ophioglossoides prevents neuronal cell death and ameliorates beta-amyloid peptide-induced memory deficits in rats.
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