First, a song by someone who should be alive, but isn't...
The above video was inspired by a Facebook friend who had an accident with Schwartzkopf black hair dye and spent ages getting the stains off her skin. You know who you are!
I may have mentioned that nutrient deficiencies can adversely affect mental (and/or other) function. Nowadays, many people live on a diet of Crap-In-A-Bag (CIAB). There's just enough essential amino acids (EAAs), essential fatty acids (EFAs), minerals & vitamins to keep their bodies alive. However, Alive ≠ Working properly.
To compensate for one (or more) nutrient deficiencies, many people are prescribed one (or more) pharmaceutical drugs to tweak how their brains work e.g. fluoxetine, citalopram/escitalopram, venlafaxine, quetiapine, risperidone, valproate etc. There are no pharmaceutical drug deficiencies!
There are people who suffer from mental (and/or other) illnesses, despite having diets & lifestyles that provide sufficient amounts of all nutrients. This post isn't about them. There are people who suffer from depression due to traumatic & inescapable events/situations. This post isn't about them, either.
Finally, nerds! We nerds love to compile information. For an interesting interview with a top compiler of useful information, see Examine's Supplement Goals Reference Guide.
For an excellent article with a mere 148 references, see Why Calories Count. To sum up:-
Where body weight is concerned, calories count (but don't bother trying to count them).
Where body composition is concerned, partitioning counts.
Where health is concerned, macronutrient ratios, EFAs, minerals, vitamins & lifestyles count.
N.B. Poor health can adversely affect body weight and/or body composition, by increasing appetite and/or by adversely affecting partitioning.
Continued on Chow on chow, Parkinson's Law, two ways of doing something, and love.
Tampilkan postingan dengan label Brain. Tampilkan semua postingan
Tampilkan postingan dengan label Brain. Tampilkan semua postingan
Can very-low-carb diets impair your mental faculties?
I wanna tell you a story...
In 2006, I had a test done on my pituitary gland*, called an Insulin Shock Test. It was pretty much what it said on the tin. I laid on a hospital bed, I was injected with an overdose of insulin and I was monitored for blood glucose and growth hormone levels every 30 minutes.
My blood glucose fell and fell and fell and fell until it reached ~1.5mmol/L (~27mg/dL). What happened was interesting. I came out in a cold sweat and developed a tremor. Apart from that, I felt fine. The consultant in charge was chatting to me and I was chatting to him. Eventually, I was given a sandwich, a yoghurt and a banana to eat.
Some time later, when I had stopped sweating and shaking, the consultant returned and told me that I had become confused. My brain had ceased to function correctly due to a lack of blood glucose (the insulin had totally suppressed serum FFAs and ketones, so there were no other brain fuels available), but I was too mentally-impaired to know that I was mentally-impaired. As far as I was concerned, everything was fine & dandy. This is the Dunning-Kruger effect.
Referring to Blood Glucose, Insulin & Diabetes, as blood glucose falls due to either starvation or a lack of dietary carbohydrate, insulin falls and glucagon rises, stimulating the liver to convert liver glycogen into glucose for export to the blood. Eventually, liver glycogen becomes depleted and blood glucose falls again. The pituitary gland notices this and secretes AdrenoCorticoTropic Hormone (ACTH) which stimulates the adrenal cortex to secrete cortisol. The adrenal glands are also stimulated to secrete adrenaline (a.k.a. epinephrine). Cortisol increases the conversion of amino acids and other substrates into glucose by the liver and kidneys. If blood glucose continues to fall, the pituitary gland secretes growth hormone (GH), which has an anti-insulin effect.
From http://anthonycolpo.com/boosting-growth-hormone-with-diet-training-fact-or-fiction-part-2/:-
"after the zero-carb phase, subjects reported symptoms of hypoglycemia that included weakness, irritability, mental confusion, nausea, hunger, cold sweating and disturbed co-ordination. GH levels were higher during exercise after the low-carb phase, but so too were levels of other fuel mobilizing hormones such as epinephrine, glucagon, and cortisol." Epinephrine, glucagon, and cortisol are stress hormones. Chronically-high blood levels of stress hormones disrupt sleep and cause irritable, aggressive behaviour.
Ethanol inhibits gluconeogenesis in the liver (possibly also in the kidneys) resulting in worse hypoglycaemia. Worse hypoglycaemia results in more ACTH & adrenaline secretion and worse hypercortisolaemia, which can adversely affect the hippocampus, impairing memory.
In conclusion, if you want to eat a very-low-carb diet, long-term:-1) Don't do much high-intensity exercise. See "Funny turns": What they aren't and what they might be.
2) Don't drink much (if any) booze.
See also Can Low-Carb Diets Make You Crazy?
*My pituitary gland failed the test by secreting only 40% the amount of GH that it was supposed to. For six months, I was given GH to inject using a special pen with a 8mm x 0.3mm needle. By the end of the six month trial, I had perfected the art of painless injection. The trial was discontinued due to lack of any noticeable benefit (17 days supply of GH @0.3mg/day cost £120!).
In 2006, I had a test done on my pituitary gland*, called an Insulin Shock Test. It was pretty much what it said on the tin. I laid on a hospital bed, I was injected with an overdose of insulin and I was monitored for blood glucose and growth hormone levels every 30 minutes.
My blood glucose fell and fell and fell and fell until it reached ~1.5mmol/L (~27mg/dL). What happened was interesting. I came out in a cold sweat and developed a tremor. Apart from that, I felt fine. The consultant in charge was chatting to me and I was chatting to him. Eventually, I was given a sandwich, a yoghurt and a banana to eat.
Some time later, when I had stopped sweating and shaking, the consultant returned and told me that I had become confused. My brain had ceased to function correctly due to a lack of blood glucose (the insulin had totally suppressed serum FFAs and ketones, so there were no other brain fuels available), but I was too mentally-impaired to know that I was mentally-impaired. As far as I was concerned, everything was fine & dandy. This is the Dunning-Kruger effect.
Referring to Blood Glucose, Insulin & Diabetes, as blood glucose falls due to either starvation or a lack of dietary carbohydrate, insulin falls and glucagon rises, stimulating the liver to convert liver glycogen into glucose for export to the blood. Eventually, liver glycogen becomes depleted and blood glucose falls again. The pituitary gland notices this and secretes AdrenoCorticoTropic Hormone (ACTH) which stimulates the adrenal cortex to secrete cortisol. The adrenal glands are also stimulated to secrete adrenaline (a.k.a. epinephrine). Cortisol increases the conversion of amino acids and other substrates into glucose by the liver and kidneys. If blood glucose continues to fall, the pituitary gland secretes growth hormone (GH), which has an anti-insulin effect.
From http://anthonycolpo.com/boosting-growth-hormone-with-diet-training-fact-or-fiction-part-2/:-
"after the zero-carb phase, subjects reported symptoms of hypoglycemia that included weakness, irritability, mental confusion, nausea, hunger, cold sweating and disturbed co-ordination. GH levels were higher during exercise after the low-carb phase, but so too were levels of other fuel mobilizing hormones such as epinephrine, glucagon, and cortisol." Epinephrine, glucagon, and cortisol are stress hormones. Chronically-high blood levels of stress hormones disrupt sleep and cause irritable, aggressive behaviour.
Ethanol inhibits gluconeogenesis in the liver (possibly also in the kidneys) resulting in worse hypoglycaemia. Worse hypoglycaemia results in more ACTH & adrenaline secretion and worse hypercortisolaemia, which can adversely affect the hippocampus, impairing memory.
In conclusion, if you want to eat a very-low-carb diet, long-term:-1) Don't do much high-intensity exercise. See "Funny turns": What they aren't and what they might be.
2) Don't drink much (if any) booze.
See also Can Low-Carb Diets Make You Crazy?
*My pituitary gland failed the test by secreting only 40% the amount of GH that it was supposed to. For six months, I was given GH to inject using a special pen with a 8mm x 0.3mm needle. By the end of the six month trial, I had perfected the art of painless injection. The trial was discontinued due to lack of any noticeable benefit (17 days supply of GH @0.3mg/day cost £120!).
PPP - another bijou rant-ette.
Blame it on the hot weather and screaming kids! :-D
PPP stands for Piss Poor Parenting.
Why, oh why, oh why do parents allow children to dictate their own diets? As if children know what's good for them! At an event I attended recently, "Johnny*" was given a plate of chicken drummers (mechanically-recovered chicken formed into the approximate shape of chicken drumsticks and coated with breadcrumbs) and oven chips. I asked Johnny if he would like a beefburger, sausage or pork steak. He replied. "I don't like them". He only wanted manufactured shite. Seriously, WTF?
When I was a lad, I was given the same food as my parents. If I didn't eat it, I went without. I ate it!
Nowadays, "children's menus" in restaurants (I'm being quite generous in the use of the word restaurant) consist of lots of manufactured shite that children like. Unlike veggies & fruit, this shite contains very little fibre/fiber or magnesium.
Is it any wonder that childhood constipation is a problem? Why are children being given PEG or even Lactulose, when there's a much better solution - Epsom Salts (which contains magnesium). The gut needs magnesium to function properly. See You're free, and a testimonial.
The brain needs magnesium to remain cool, calm and collected i.e. function properly. The brain also needs DHA and Vitamin D3 to function properly. Many kids don't like oily fish so they won't/don't eat it. It's not rocket science to purée some wild red salmon with some Bolognese/Sweet chilli/w.h.y. sauce so that they won't notice it. Many kids play indoors or are smothered in sunblock when they do go outdoors. Is it any wonder that childhood ADD/ADHD is much more common? Medication and psychotherapy? Seriously, WTF?
When I was a lad, there were a couple of show-offs in my class at school, but nobody behaved like "Jimmy*" (physically and mentally hyperactive with bad behaviour, screaming and shouting). Johnny was also badly behaved, but not as bad as Jimmy. The parents at the event seemed content that, every day, their children had to be given "uppers" (e.g. Ritalin) to help them concentrate during the day and "downers" to help them sleep at night. Seriously, WTF?
I will now take a deep breath and count to twenty. There, that's better!
*Names changed.
Why, oh why, oh why do parents allow children to dictate their own diets? As if children know what's good for them! At an event I attended recently, "Johnny*" was given a plate of chicken drummers (mechanically-recovered chicken formed into the approximate shape of chicken drumsticks and coated with breadcrumbs) and oven chips. I asked Johnny if he would like a beefburger, sausage or pork steak. He replied. "I don't like them". He only wanted manufactured shite. Seriously, WTF?
When I was a lad, I was given the same food as my parents. If I didn't eat it, I went without. I ate it!
Nowadays, "children's menus" in restaurants (I'm being quite generous in the use of the word restaurant) consist of lots of manufactured shite that children like. Unlike veggies & fruit, this shite contains very little fibre/fiber or magnesium.
Is it any wonder that childhood constipation is a problem? Why are children being given PEG or even Lactulose, when there's a much better solution - Epsom Salts (which contains magnesium). The gut needs magnesium to function properly. See You're free, and a testimonial.
The brain needs magnesium to remain cool, calm and collected i.e. function properly. The brain also needs DHA and Vitamin D3 to function properly. Many kids don't like oily fish so they won't/don't eat it. It's not rocket science to purée some wild red salmon with some Bolognese/Sweet chilli/w.h.y. sauce so that they won't notice it. Many kids play indoors or are smothered in sunblock when they do go outdoors. Is it any wonder that childhood ADD/ADHD is much more common? Medication and psychotherapy? Seriously, WTF?
When I was a lad, there were a couple of show-offs in my class at school, but nobody behaved like "Jimmy*" (physically and mentally hyperactive with bad behaviour, screaming and shouting). Johnny was also badly behaved, but not as bad as Jimmy. The parents at the event seemed content that, every day, their children had to be given "uppers" (e.g. Ritalin) to help them concentrate during the day and "downers" to help them sleep at night. Seriously, WTF?
I will now take a deep breath and count to twenty. There, that's better!
*Names changed.
Get in! Part 4. Get out! Get this!
First, here's a rather jolly but not safe for work song from The Beautiful South.
Mum's GP has approved mum getting 500mg/day Thiamine. I'm waiting for it to arrive from Vitacost.
Mum's GP has approved the discontinuation of Aspirin 75mg/day and Omeprazole 20mg/day, as they are of little benefit and it reduces the number of pills that mum has to swallow each day.
I sang backing vocals for my friend Ray Langstone with a group of excellent musicians at the Unicorn pub on Monday evening. That's the first time I've done something like that.
This is the song Ray sang.
Mum's GP has approved mum getting 500mg/day Thiamine. I'm waiting for it to arrive from Vitacost.
Mum's GP has approved the discontinuation of Aspirin 75mg/day and Omeprazole 20mg/day, as they are of little benefit and it reduces the number of pills that mum has to swallow each day.
I sang backing vocals for my friend Ray Langstone with a group of excellent musicians at the Unicorn pub on Monday evening. That's the first time I've done something like that.
This is the song Ray sang.
Look after your brain, Part 5.
This is another bookmarking post.
I spotted an article by Emily Deans M.D. called Nutritional Brain Bomb - Thiamine Deficiency.
So there's yet another way to knacker the brain, resulting in Wernicke's encephalopathy and in severe cases, Korsakoff's psychosis. Both of these conditions are partially irreversible due to neuron death. Both of these conditions are partially reversible by high-dose thiamine therapy.
Thiamine 500mg/day is one last therapy to try mum on after I've got her back on Vitamin K2 (hopefully today).
Continued on Quality >> Quantity.
I spotted an article by Emily Deans M.D. called Nutritional Brain Bomb - Thiamine Deficiency.
So there's yet another way to knacker the brain, resulting in Wernicke's encephalopathy and in severe cases, Korsakoff's psychosis. Both of these conditions are partially irreversible due to neuron death. Both of these conditions are partially reversible by high-dose thiamine therapy.
Thiamine 500mg/day is one last therapy to try mum on after I've got her back on Vitamin K2 (hopefully today).
Continued on Quality >> Quantity.
Use 'em or lose 'em, Part 2.
I'm talking about your brain(s). Last year, I became depressed for several months for personal reasons that I won't go into. On December 8th 2011, something happened and the depression went away in an instant.
Unfortunately, several months of lying around doing very little had turned my brain to stodge. I tentatively resumed blogging in January 2012.
I find that the more I use my brain, the better it works, the more I can remember and the more I want to use it.
On the minus side, I find that I'm more impatient than I used to be. I'm now quite intolerant of, erm, f***wits on the roads and on the internets. Don't mention Giant Pandas!
At first I was afraid, I was petrified...
My titles are becoming increasingly blatantly song-orientated. No YouTube video, this time.
I just read Hans Wu's latest post Alzheimer's and Dementia and had a few thoughts.
1) In the early stages of mental decline, there is still self-awareness and the process is frightening. Constant reassurance is the best thing for somebody in this state. As self-awareness fades, one becomes happy. An example of this is HAL-9000 as his memory modules were being unplugged in the film "2001 a space odyssey". My mum is in this state, thank goodness.
I entered this state temporarily during an Insulin Shock Test on my pituitary gland, when my serum glucose fell to 1.5mmol/L (27mg/dL) under medical supervision. I was blissfully unaware of my confusion. Too much alcohol in the blood also causes loss of self-awareness. I entered this state last week while socialising with a friend. After half a bottle of White Zinfandel, I was blissfully unaware of my merriness!
2) When I see "arterial stiffness", I think "inappropriate calcification" and "Vitamin K2".
3) Transient Ischaemic Attacks (TIAs a.k.a. mini-strokes) cause loss of blood flow to parts of the brain, resulting in amnesia. There may be some permanent brain damage, depending on how long the TIAs last. TIAs can be caused by spasms in arteries within the brain. Ditto migraines.
When I see "spasm", I think "magnesium".
I just read Hans Wu's latest post Alzheimer's and Dementia and had a few thoughts.
1) In the early stages of mental decline, there is still self-awareness and the process is frightening. Constant reassurance is the best thing for somebody in this state. As self-awareness fades, one becomes happy. An example of this is HAL-9000 as his memory modules were being unplugged in the film "2001 a space odyssey". My mum is in this state, thank goodness.
I entered this state temporarily during an Insulin Shock Test on my pituitary gland, when my serum glucose fell to 1.5mmol/L (27mg/dL) under medical supervision. I was blissfully unaware of my confusion. Too much alcohol in the blood also causes loss of self-awareness. I entered this state last week while socialising with a friend. After half a bottle of White Zinfandel, I was blissfully unaware of my merriness!
2) When I see "arterial stiffness", I think "inappropriate calcification" and "Vitamin K2".
3) Transient Ischaemic Attacks (TIAs a.k.a. mini-strokes) cause loss of blood flow to parts of the brain, resulting in amnesia. There may be some permanent brain damage, depending on how long the TIAs last. TIAs can be caused by spasms in arteries within the brain. Ditto migraines.
When I see "spasm", I think "magnesium".
Reasons to get moving...
First, a music video. What else but...?
Part 1. Get slimmer.
Insulin increases the amount of nutrients entering adipocytes, which makes us fat and hungry.
Er, just a minute!
If increasing the amount of nutrients entering cells makes us hungry, exercise (which increases the amount of nutrients entering muscle cells) would make us hungry. It doesn't. See Fig. 1. in Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males.
If going for a walk outdoors makes you hungry, you're doing it wrong. Wrap up warm, as feeling cold increases hunger. Low blood glucose level also increases hunger, so don't over-exercise while on a long-term ketogenic diet.
By the way, insulin also increases the amount of nutrients entering muscle cells.
Q. What determines the relative amounts of nutrients entering adipocytes vs muscle cells?
A. The relative insulin sensitivities of adipocytes vs muscle cells.
Adipocytes are sensitive to insulin until they become full. To reduce the amount of nutrients entering adipocytes, divert more nutrients to muscle cells by increasing their insulin sensitivity. Emptying muscle cells by doing low-intensity exercise increases their insulin sensitivity. High-intensity exercise increases their insulin sensitivity.
Part 2. Prevent/reverse age-related sarcopenia (muscle loss).
See Use 'em or lose 'em. As diverting more nutrients to muscle cells increases muscle mass, increasing their insulin sensitivity results in increased muscle mass, unless you're eating way below maintenance calories. High-intensity exercise results in more muscle mass gain than low-intensity exercise.
Part 3. Make your brain work properly.
Thanks to Chris Highcock, who gave me a complimentary copy of Hillfit, I found IL-6 and IL-10 Anti-Inflammatory Activity Links Exercise to Hypothalamic Insulin and Leptin Sensitivity through IKKβ and ER Stress Inhibition.
In plain English, this means that exercise increases both insulin and leptin sensitivity in the hypothalamus. As the hypothalamus controls appetite and both insulin & leptin are appetite-suppressing, the net result is less appetite.
Part 1. Get slimmer.
Insulin increases the amount of nutrients entering adipocytes, which makes us fat and hungry.
Er, just a minute!
If increasing the amount of nutrients entering cells makes us hungry, exercise (which increases the amount of nutrients entering muscle cells) would make us hungry. It doesn't. See Fig. 1. in Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males.
If going for a walk outdoors makes you hungry, you're doing it wrong. Wrap up warm, as feeling cold increases hunger. Low blood glucose level also increases hunger, so don't over-exercise while on a long-term ketogenic diet.
By the way, insulin also increases the amount of nutrients entering muscle cells.
Q. What determines the relative amounts of nutrients entering adipocytes vs muscle cells?
A. The relative insulin sensitivities of adipocytes vs muscle cells.
Adipocytes are sensitive to insulin until they become full. To reduce the amount of nutrients entering adipocytes, divert more nutrients to muscle cells by increasing their insulin sensitivity. Emptying muscle cells by doing low-intensity exercise increases their insulin sensitivity. High-intensity exercise increases their insulin sensitivity.
Part 2. Prevent/reverse age-related sarcopenia (muscle loss).
See Use 'em or lose 'em. As diverting more nutrients to muscle cells increases muscle mass, increasing their insulin sensitivity results in increased muscle mass, unless you're eating way below maintenance calories. High-intensity exercise results in more muscle mass gain than low-intensity exercise.
Part 3. Make your brain work properly.
Thanks to Chris Highcock, who gave me a complimentary copy of Hillfit, I found IL-6 and IL-10 Anti-Inflammatory Activity Links Exercise to Hypothalamic Insulin and Leptin Sensitivity through IKKβ and ER Stress Inhibition.
In plain English, this means that exercise increases both insulin and leptin sensitivity in the hypothalamus. As the hypothalamus controls appetite and both insulin & leptin are appetite-suppressing, the net result is less appetite.
Dementia: A review of the evidence.
To make my discussions with Health Professionals a.k.a. "experts" more effective, I need to know what they know. To help me with this task, I have been rummaging through The Cochrane Library. The results for Dementia NOT "Down Syndrome" NOT Vascular NOT Aids NOT carer and Reviews only produced 44 results. Some weren't relevant. The following are relevant and I have added the plain language summary:-
Acetyl-l-carnitine for dementia. No evidence of benefit of Acetyl-l-carnitine for dementia.
Alpha lipoic acid for dementia. No evidence of efficacy of alpha lipoic acid for dementia.
Antidepressants for treating depression in dementia. Insufficient evidence for the efficacy and safety of antidepressants for depression in dementia.
Aroma therapy for dementia. The one small trial published is insufficient evidence for the efficacy of aroma therapy for dementia.
Cannabinoids for the treatment of dementia. No evidence that cannabinoids are effective in the improvement of disturbed behaviour in dementia or in the treatment of other symptoms of dementia.
Cholinesterase inhibitors for dementia with Lewy bodies. No convincing evidence from one trial of the efficacy of cholinesterase inhibitors for dementia with Lewy bodies.
Cholinesterase inhibitors for Parkinson's disease dementia. Rivastigmine appears to moderately improve cognition and to a lesser extent activities of daily living in patients with PDD.
Donepezil for dementia due to Alzheimer's disease. Donepezil is beneficial for people with mild, moderate and severe dementia due to Alzheimer's disease.
Ginkgo biloba for cognitive impairment and dementia. There is no convincing evidence that Ginkgo biloba is efficacious for dementia and cognitive impairment.
Haloperidol for agitation in dementia. No evidence has been found of any significant general improvement in manifestations of agitation, other than aggression, among demented patients treated with haloperidol, compared with controls.
Homeopathy for dementia. No evidence that homeopathy is effective in treating dementia.
Hormone replacement therapy to maintain cognitive function in women with dementia. There is no evidence of a positive effect that oestrogen replacement therapy can maintain cognitive function for a longer period of time (> five months) in women with Alzheimer's disease.
Hydergine for dementia. Uncertainty about the efficacy of hydergine in dementia.
Lecithin for dementia and cognitive impairment. Doubtful effect of lecithin as a treatment for dementia.
Light therapy for managing cognitive, sleep, functional, behavioural, or psychiatric disturbances in dementia. There is insufficient evidence to determine whether light therapy is effective in the management of cognitive, sleep, functional, behavioural or psychiatric disturbances in dementia.
Massage and touch for dementia. Insufficient evidence to draw conclusions about the possibility that massage and touch interventions are effective for dementia or associated problems.
Memantine for dementia. Some evidence of efficacy of memantine for dementia.
Music therapy for people with dementia. There is no substantial evidence to support nor discourage the use of music therapy in the care of older people with dementia.
Nicergoline for dementia and other age associated forms of cognitive impairment. Nicergoline may improve cognition and behavioural function of people with mild to moderate dementia.
Omega 3 fatty acid for the prevention of dementia. There is no evidence that dietary or supplemental omega 3 polyunsaturated fatty acid (PUFA) reduces the risk of cognitive impairment or dementia in healthy elderly persons without pre-existing dementia. This review yielded no clinical trials that could confirm or refute the utility of omega 3 PUFA in preventing cognitive impairment or dementia. This is an important area that is in pressing need of further research.
Physical activity programs for persons with dementia. There is insufficient evidence to determine the effectiveness of physical activity programs in managing or improving cognition, function, behaviour, depression, and mortality in people with dementia.
Physostigmine for dementia due to Alzheimer's disease. Limited evidence of effectiveness of physostigmine for the symptomatic treatment of Alzheimer's disease.
Piracetam for dementia or cognitive impairment. Evidence for the efficacy of piracetam for dementia or cognitive impairment is inadequate for clinical use but sufficient to justify further research.
Procaine treatments for cognition and dementia. In analysing the effect of procaine and its preparations, there was no evidence for benefit in the prevention or treatment of dementia or cognitive impairment.
Propentofylline for dementia. Limited evidence that propentofylline benefits cognition, global function and activities of daily living in people with Alzheimer's disease and/or vascular dementia.
Reminiscence therapy for dementia. Inconclusive evidence of the efficacy of reminiscence therapy for dementia.
Snoezelen for dementia. No evidence of the efficacy of snoezelen or multi-sensory stimulation programmes for people with dementia.
Statins for the prevention of dementia. There (is) good evidence that statins given in late life to individuals at risk of vascular disease have no effect in preventing dementia.
Thioridazine for dementia. No evidence to support the use of thioridazine for dementia.
Transcutaneous Electrical Nerve Stimulation (TENS) for dementia. Insufficient data to determine the efficacy of transcutaneous electrical nerve stimulation for dementia.
Trazodone for agitation in dementia. Insufficient evidence from randomized, placebo-controlled studies to support a recommendation that trazodone should be prescribed, or not prescribed, for BPSD.
Validation therapy for dementia. No new evidence of the efficacy of validation therapy for people with dementia or cognitive impairment has been identified.
Valproate preparations for agitation in dementia. No evidence of efficacy of valproate preparations for treatment of agitation in people with dementia.
Vinpocetine for cognitive impairment and dementia. Insufficient evidence of benefits of vinpocetine for people with dementia.
So there you have it. Virtually everything that's been thoroughly tested is ineffective for the treatment of dementia.
There are a whole load of things that haven't been properly tested yet e.g. Omega-3, Vitamin D3, Vitamin K2, Curcumin, Berberine, Trans-dermal Progesterone, Sub-lingual B12, S-Adeno-Methionine and The Ketogenic Diet. What is The Alzheimer's Society doing with all of the money that they get?
Finally, I accept that mum is on her last legs and won't be around for much longer, so here's a song. I normally hate raps, but the Pinky & Perky backing vocals are kinda quirky and the lyrics are poignant. So here's Stay with Me by DJ Ironik. Listen to the words!
Acetyl-l-carnitine for dementia. No evidence of benefit of Acetyl-l-carnitine for dementia.
Alpha lipoic acid for dementia. No evidence of efficacy of alpha lipoic acid for dementia.
Antidepressants for treating depression in dementia. Insufficient evidence for the efficacy and safety of antidepressants for depression in dementia.
Aroma therapy for dementia. The one small trial published is insufficient evidence for the efficacy of aroma therapy for dementia.
Cannabinoids for the treatment of dementia. No evidence that cannabinoids are effective in the improvement of disturbed behaviour in dementia or in the treatment of other symptoms of dementia.
Cholinesterase inhibitors for dementia with Lewy bodies. No convincing evidence from one trial of the efficacy of cholinesterase inhibitors for dementia with Lewy bodies.
Cholinesterase inhibitors for Parkinson's disease dementia. Rivastigmine appears to moderately improve cognition and to a lesser extent activities of daily living in patients with PDD.
Donepezil for dementia due to Alzheimer's disease. Donepezil is beneficial for people with mild, moderate and severe dementia due to Alzheimer's disease.
Ginkgo biloba for cognitive impairment and dementia. There is no convincing evidence that Ginkgo biloba is efficacious for dementia and cognitive impairment.
Haloperidol for agitation in dementia. No evidence has been found of any significant general improvement in manifestations of agitation, other than aggression, among demented patients treated with haloperidol, compared with controls.
Homeopathy for dementia. No evidence that homeopathy is effective in treating dementia.
Hormone replacement therapy to maintain cognitive function in women with dementia. There is no evidence of a positive effect that oestrogen replacement therapy can maintain cognitive function for a longer period of time (> five months) in women with Alzheimer's disease.
Hydergine for dementia. Uncertainty about the efficacy of hydergine in dementia.
Lecithin for dementia and cognitive impairment. Doubtful effect of lecithin as a treatment for dementia.
Light therapy for managing cognitive, sleep, functional, behavioural, or psychiatric disturbances in dementia. There is insufficient evidence to determine whether light therapy is effective in the management of cognitive, sleep, functional, behavioural or psychiatric disturbances in dementia.
Massage and touch for dementia. Insufficient evidence to draw conclusions about the possibility that massage and touch interventions are effective for dementia or associated problems.
Memantine for dementia. Some evidence of efficacy of memantine for dementia.
Music therapy for people with dementia. There is no substantial evidence to support nor discourage the use of music therapy in the care of older people with dementia.
Nicergoline for dementia and other age associated forms of cognitive impairment. Nicergoline may improve cognition and behavioural function of people with mild to moderate dementia.
Omega 3 fatty acid for the prevention of dementia. There is no evidence that dietary or supplemental omega 3 polyunsaturated fatty acid (PUFA) reduces the risk of cognitive impairment or dementia in healthy elderly persons without pre-existing dementia. This review yielded no clinical trials that could confirm or refute the utility of omega 3 PUFA in preventing cognitive impairment or dementia. This is an important area that is in pressing need of further research.
Physical activity programs for persons with dementia. There is insufficient evidence to determine the effectiveness of physical activity programs in managing or improving cognition, function, behaviour, depression, and mortality in people with dementia.
Physostigmine for dementia due to Alzheimer's disease. Limited evidence of effectiveness of physostigmine for the symptomatic treatment of Alzheimer's disease.
Piracetam for dementia or cognitive impairment. Evidence for the efficacy of piracetam for dementia or cognitive impairment is inadequate for clinical use but sufficient to justify further research.
Procaine treatments for cognition and dementia. In analysing the effect of procaine and its preparations, there was no evidence for benefit in the prevention or treatment of dementia or cognitive impairment.
Propentofylline for dementia. Limited evidence that propentofylline benefits cognition, global function and activities of daily living in people with Alzheimer's disease and/or vascular dementia.
Reminiscence therapy for dementia. Inconclusive evidence of the efficacy of reminiscence therapy for dementia.
Snoezelen for dementia. No evidence of the efficacy of snoezelen or multi-sensory stimulation programmes for people with dementia.
Statins for the prevention of dementia. There (is) good evidence that statins given in late life to individuals at risk of vascular disease have no effect in preventing dementia.
Thioridazine for dementia. No evidence to support the use of thioridazine for dementia.
Transcutaneous Electrical Nerve Stimulation (TENS) for dementia. Insufficient data to determine the efficacy of transcutaneous electrical nerve stimulation for dementia.
Trazodone for agitation in dementia. Insufficient evidence from randomized, placebo-controlled studies to support a recommendation that trazodone should be prescribed, or not prescribed, for BPSD.
Validation therapy for dementia. No new evidence of the efficacy of validation therapy for people with dementia or cognitive impairment has been identified.
Valproate preparations for agitation in dementia. No evidence of efficacy of valproate preparations for treatment of agitation in people with dementia.
Vinpocetine for cognitive impairment and dementia. Insufficient evidence of benefits of vinpocetine for people with dementia.
So there you have it. Virtually everything that's been thoroughly tested is ineffective for the treatment of dementia.
There are a whole load of things that haven't been properly tested yet e.g. Omega-3, Vitamin D3, Vitamin K2, Curcumin, Berberine, Trans-dermal Progesterone, Sub-lingual B12, S-Adeno-Methionine and The Ketogenic Diet. What is The Alzheimer's Society doing with all of the money that they get?
Finally, I accept that mum is on her last legs and won't be around for much longer, so here's a song. I normally hate raps, but the Pinky & Perky backing vocals are kinda quirky and the lyrics are poignant. So here's Stay with Me by DJ Ironik. Listen to the words!
Look after your brain, Part 4.
Ketogenic Diet REALLY WORKS!!!
WHAT IF THERE WAS A CURE FOR ALZHEIMER’S DISEASE AND NO ONE KNEW?
High fat, low carb diet may help Alzheimer's sufferers.
The above popped-up when I Googled for "ketogenic diet" alzheimer's.
See also
D-β-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease ,
D-β-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson disease ,
Ketones: Metabolism's ugly duckling ,
Ketone bodies, potential therapeutic uses ,
Neuroprotective and disease-modifying effects of the ketogenic diet ,
Ketone bodies as a therapeutic for Alzheimer's disease ,
Altered lipid metabolism in brain injury and disorders ,
The ketogenic diet: uses in epilepsy and other neurologic illnesses and
Branched chain amino acids as adjunctive therapy to ketogenic diet in epilepsy: pilot study and hypothesis.
EDIT: Ketones give the brain two fuels to run on instead of one (glucose). This improves mental function considerably. However, it can't repair the damage done to the brain by amyloid plaques, protein tangles etc. Sadly, this damage is progressive and permanent. Therefore, coconut oil can't cure Alzheimer's Disease, Lewy Body Dementia etc. It just delays the inevitable.
It's mum's 80th Birthday today so I'm off to see her now.
Continued on Look after your brain, Part 5.
WHAT IF THERE WAS A CURE FOR ALZHEIMER’S DISEASE AND NO ONE KNEW?
High fat, low carb diet may help Alzheimer's sufferers.
The above popped-up when I Googled for "ketogenic diet" alzheimer's.
See also
D-β-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease ,
D-β-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson disease ,
Ketones: Metabolism's ugly duckling ,
Ketone bodies, potential therapeutic uses ,
Neuroprotective and disease-modifying effects of the ketogenic diet ,
Ketone bodies as a therapeutic for Alzheimer's disease ,
Altered lipid metabolism in brain injury and disorders ,
The ketogenic diet: uses in epilepsy and other neurologic illnesses and
Branched chain amino acids as adjunctive therapy to ketogenic diet in epilepsy: pilot study and hypothesis.
EDIT: Ketones give the brain two fuels to run on instead of one (glucose). This improves mental function considerably. However, it can't repair the damage done to the brain by amyloid plaques, protein tangles etc. Sadly, this damage is progressive and permanent. Therefore, coconut oil can't cure Alzheimer's Disease, Lewy Body Dementia etc. It just delays the inevitable.
It's mum's 80th Birthday today so I'm off to see her now.
Continued on Look after your brain, Part 5.
Look after your brain, Part 3.
Funnily enough, on the Mean Forum that I mentioned in my previous post and in the very same discussion, someone suggested two supplements of which I was unaware that can improve mental function.
1) SAMe (S-adenosyl-methionine). See S-adenosyl methionine: a natural therapeutic agent effective against multiple hallmarks and risk factors associated with Alzheimer's Disease and Polyunsaturated fatty acid and S-adenosylmethionine supplementation in predementia syndromes and Alzheimer's Disease: a review.
2) Methylcobalamin, sublingual. See From mild cognitive impairment to Alzheimer's Disease - influence of homocysteine, vitamin B12 and folate on cognition over time: results from one-year follow-up and Cumulative incidence of vitamin B12 deficiency in patients with Alzheimer's Disease.
Vitamin B12 should be taken sub-lingually (or nasally), as old people's stomachs secrete less Intrinsic Factor (required for B12 absorption in the gut) than young people's. Old people who take a Proton Pump Inhibitor (***prazole) for acid reflux secrete even less Intrinsic Factor still.
I will give these a try.
Continued on Look after your brain, Part 4.
1) SAMe (S-adenosyl-methionine). See S-adenosyl methionine: a natural therapeutic agent effective against multiple hallmarks and risk factors associated with Alzheimer's Disease and Polyunsaturated fatty acid and S-adenosylmethionine supplementation in predementia syndromes and Alzheimer's Disease: a review.
2) Methylcobalamin, sublingual. See From mild cognitive impairment to Alzheimer's Disease - influence of homocysteine, vitamin B12 and folate on cognition over time: results from one-year follow-up and Cumulative incidence of vitamin B12 deficiency in patients with Alzheimer's Disease.
Vitamin B12 should be taken sub-lingually (or nasally), as old people's stomachs secrete less Intrinsic Factor (required for B12 absorption in the gut) than young people's. Old people who take a Proton Pump Inhibitor (***prazole) for acid reflux secrete even less Intrinsic Factor still.
I will give these a try.
Continued on Look after your brain, Part 4.
Look after your brain, Part 2.
Mum used to use a transdermal Natural Progesterone Cream (to reverse hair loss) but she stopped using it some time before she became mentally impaired. I found a half-full pot of the stuff in mum's house and have instructed the nursing staff to rub a blob of cream on mum's skin each day to see if it makes any improvement to her Lewy Body Dementia. See Regeneration in a degenerating brain: potential of allopregnanolone as a neuroregenerative agent , Regenerative potential of allopregnanolone and Progesterone receptors: form and function in brain.
Getting mum to eat more smoked salmon has definitely perked her up. I've also managed to re-introduce turmeric into her diet (she was spitting out the turmeric pills as they were large & unchewable) by getting the nursing staff to stir a teaspoonful of turmeric powder into her orange juice (I & she can't taste it) once every few days. Luckily, she never had any problems taking the Vitamin D3 & K2 capsules/gelcaps.
Finally, I'm trying to get mum on low dose Aspirin, as Aspirin inhibits the aggregation of proteins (synuclein, beta amyloid) on charged polymers in amyloid diseases, such as Parkinson’s disease, Alzheimer’s disease, etc., according to Dr Art Ayers. As mum has a hiatus hernia, which causes acid reflux, her GP may not allow her to do this even though mum is taking a Proton Pump Inhibitor and Gaviscon. See The role of anti-inflammatory drugs in the prevention and treatment of Alzheimer's disease and Non-steroidal anti-inflammatory drugs (NSAIDs) and other anti-inflammatory agents in the treatment of neurodegenerative disease.
Continued on Look after your brain, Part 3.
Getting mum to eat more smoked salmon has definitely perked her up. I've also managed to re-introduce turmeric into her diet (she was spitting out the turmeric pills as they were large & unchewable) by getting the nursing staff to stir a teaspoonful of turmeric powder into her orange juice (I & she can't taste it) once every few days. Luckily, she never had any problems taking the Vitamin D3 & K2 capsules/gelcaps.
Finally, I'm trying to get mum on low dose Aspirin, as Aspirin inhibits the aggregation of proteins (synuclein, beta amyloid) on charged polymers in amyloid diseases, such as Parkinson’s disease, Alzheimer’s disease, etc., according to Dr Art Ayers. As mum has a hiatus hernia, which causes acid reflux, her GP may not allow her to do this even though mum is taking a Proton Pump Inhibitor and Gaviscon. See The role of anti-inflammatory drugs in the prevention and treatment of Alzheimer's disease and Non-steroidal anti-inflammatory drugs (NSAIDs) and other anti-inflammatory agents in the treatment of neurodegenerative disease.
Continued on Look after your brain, Part 3.
Guess who didn't look after his brain?
Due to the sudden deterioration in my mum's physical & mental health and also due to struggling to come to terms with her having to spend the rest of her life in a nursing home (not the happiest of places), my diet went completely to pot.
I "went off" salmon, sardines & powdered linseeds and started to eat carbohydrate/fat-based comfort foods. A black cloud slowly descended over me. I lost the motivation to do anything, including updating this blog. I also slept a lot. This continued for several months.
Then, for no apparent reason, a few weeks ago I got an urge to eat smoked salmon. I added 200g of smoked salmon twice a week back into my diet and after a few weeks, the black cloud started to lift.
Before I started supplementing with Vitamin D3, I used to eat lots of oily fish but did not function correctly mentally. This time, my Vitamin D3 status was good (I never stopped taking supplements even when I had the black cloud over me) but my EPA (Eicosapentaenoic Acid) and DHA (Docosahexaenoic Acid) intakes were near zero.
In conclusion, it would appear that my brain needs adequate Vitamin D3 and EPA and DHA (and magnesium) to function correctly.
I won't be blogging as much as I have been previously, as I've now dumped the vast majority of the nutritional knowledge within my brain into this blog. If I come across anything new, I'll post it here.
Finally, I've found the cheapest source yet of 5,000iu Vitamin D3 gelcaps.
I "went off" salmon, sardines & powdered linseeds and started to eat carbohydrate/fat-based comfort foods. A black cloud slowly descended over me. I lost the motivation to do anything, including updating this blog. I also slept a lot. This continued for several months.
Then, for no apparent reason, a few weeks ago I got an urge to eat smoked salmon. I added 200g of smoked salmon twice a week back into my diet and after a few weeks, the black cloud started to lift.
Before I started supplementing with Vitamin D3, I used to eat lots of oily fish but did not function correctly mentally. This time, my Vitamin D3 status was good (I never stopped taking supplements even when I had the black cloud over me) but my EPA (Eicosapentaenoic Acid) and DHA (Docosahexaenoic Acid) intakes were near zero.
In conclusion, it would appear that my brain needs adequate Vitamin D3 and EPA and DHA (and magnesium) to function correctly.
I won't be blogging as much as I have been previously, as I've now dumped the vast majority of the nutritional knowledge within my brain into this blog. If I come across anything new, I'll post it here.
Finally, I've found the cheapest source yet of 5,000iu Vitamin D3 gelcaps.
Look after your brain.
"One in three people over 65 will die with dementia..." said Dr Susanne Sorensen, head of research at the Alzheimer's Society. I read this in a recent BBC News article Vitamin D 'is mental health aid' which referred to the study Serum 25-Hydroxyvitamin D Concentration and Cognitive Impairment.
The article contained the usual phrase "...more work was needed..."
The above article also led to Parkinson's linked to vitamin D which referred to the study Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease. "However, the Emory University researchers do not yet know if the vitamin deficiency is a cause or the result of having Parkinson's". "Further research is required...." yet again.
It's like someone standing by their broken-down car wondering whether it's the empty fuel tank that's made the car stop or whether it's the car stopping that's made the fuel tank empty. Does it matter? Just put some fuel in the tank and see what happens! See also Higher serum vitamin D3 levels are associated with better cognitive test performance in patients with Alzheimer's disease.
Severe Mental Impairment blights the lives of many old people and their loved ones. My mum developed Parkinson's Disease a few years ago. I didn't know anything about the condition at the time, but it's caused by the formation of Lewy Bodies (blobs of abnormally-folded alpha-synuclein protein) in the substantia nigra part of the brain, which controls movement. This part of the brain has high levels of the Vitamin D receptor. Why does the brain contain Vitamin D receptors?
As Lewy Bodies form in other parts of the brain, mental faculties decline. The hippocampus is involved with short-term memory. The neocortex is involved with concious thought.
Mum started showing obvious signs of mental impairment in August 2007. She was assessed by a Community Psychiatric Nurse (CPN) in January 2008 when she scored 14/30 in a MMSE. She was unable to remember 3 words or follow 2 simple instructions in a row (e.g. fold this piece of paper in half and put it on the floor). I started her on 5,000iu/day of Vitamin D3 as it was having a positive effect on my mental function. She was prescribed Aricept, starting at 5mg/day for a month then increasing to 10mg/day. In May 2008 she was re-assessed and scored 26/30 in a MMSE. EDIT: In 2010, Mum's consultant told me that Aricept increases MMSE score by 3 points on average.
Unfortunately, Aricept has side-effects including severe diarrhoea and worsening of the symptoms of Parkinson's Disease which she complained about, so her Aricept dose was reduced back to 5mg/day.
Unsurprisingly, this resulted in a slight decline in mum's mental faculties. In November 2008, I increased her intake of smoked salmon to about 400g/week, as the consumption of long-chain pufas have benefits. See
Low Plasma N-3 Fatty Acids and Dementia in Older Persons: The InCHIANTI Study and
Disruption of glial (oligodendrocyte and astrocyte) cellular function leads to carnosine (b-alanyl-L-histidine) synthesis failure, and nutrient and protective factor deficiency in neurons with secondary development of oxidative stress and amyloid toxicity, with subsequent neuronal dysfunction and development of dementia which stated "Measures which reduce toxicity to vascular endothelium and glia, such as fish oil, may have potential for reducing the likelihood of development of the disease..."
After about four weeks, this had a noticeable (by myself and mum's friend) positive effect on her mental faculties so, inspired by Dr Art Ayers, I started her on Turmeric (curcumin) extract and Goldenseal (berberine) extract. See
Curcumin inhibits aggregation of alpha-synuclein
Neuroprotective effects of curcumin
Alpha-synuclein assembly as a therapeutic target of Parkinson's disease and related disorders
Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model
Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers
Research on the mechanism of neuronal apoptosis in Alzheimer's disease and the effects of tetrohydroberberine on the apoptosis... and
Berberine chloride can ameliorate the spatial memory impairment and increase the expression of interleukin-1beta and inducible nitric oxide synthase in the rat model of Alzheimer's disease.
On January 12th 2009, mum was re-assessed and scored 26/30 in a MMSE. I thought that this was impressive considering that a) she was taking half the dose of Aricept compared to when she previously got that score, b) she had no adverse effects from taking any of the supplements and c) she was 8 months older and degenerative brain diseases worsen with time.
I mentioned to the CPN who did the MMSE that I was starting mum on 15mg/week Vitamin K2 as there were benefits. See
Menaquinone-4 concentration is correlated with sphingolipid concentrations in rat brain ,
Vitamin K status influences brain sulfatide metabolism in young mice and rats ,
Vitamin K and sphingolipid metabolism: evidence to date ,
Substantial sulfatide deficiency and ceramide elevation in very early Alzheimer's disease: potential role in disease pathogenesis and
The possible role of vitamin K deficiency in the pathogenesis of Alzheimer's disease and in augmenting brain damage associated with cardiovascular disease
I don't know what sphingolipids are (I know who probably does) but sulfatides are good and ceramides are bad.
Around the time that mum collapsed, I received a copy of a letter from the CPN to mum's GP which stated "I have informed him (i.e. me) that I am unaware of any robust evidence that these substances are of any benefit." However, there is no evidence that these substances are of any harm.
And finally......
What started the cascade of confusion and collapse leading to hospitalisation and discharge to a nursing home was a simple Urinary Tract Infection (UTI) of e. coli. I don't know why UTIs cause so much confusion in elderly people, but elderly females are at a high risk of developing UTIs because a) elderly people don't drink enough so they don't pass enough urine, b) females have insufficient spacing between anus & urethra and c) elderly females who have any urinary/faecal leakage wear a Tena disposable "nappy/diaper", which increases the likelihood of faeces entering the urethra.
To reduce the risk of further UTIs, I have supplied the nursing home with a pot of D-mannose Plus, which contains d-mannose and cranberry extract, with instructions to add a heaped teaspoonful to a glass of juice once a week. See Intervening with urinary tract infections using anti-adhesives based on the crystal structure of the FimH-oligomannose-3 complex and
Natural approaches to prevention and treatment of infections of the lower urinary tract
EDIT: Thanks to Galina L for bringing the following study to my attention.
Magnesium supplementation in the treatment of dementia patients.
It's probably of no help to Lewy Body Dementia sufferers, as they already have high Mg levels in their CSF. See CSF Mg and Ca as diagnostic markers for dementia with Lewy bodies.
Continued on Look after your brain, Part 2.
The article contained the usual phrase "...more work was needed..."
The above article also led to Parkinson's linked to vitamin D which referred to the study Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease. "However, the Emory University researchers do not yet know if the vitamin deficiency is a cause or the result of having Parkinson's". "Further research is required...." yet again.
It's like someone standing by their broken-down car wondering whether it's the empty fuel tank that's made the car stop or whether it's the car stopping that's made the fuel tank empty. Does it matter? Just put some fuel in the tank and see what happens! See also Higher serum vitamin D3 levels are associated with better cognitive test performance in patients with Alzheimer's disease.
Severe Mental Impairment blights the lives of many old people and their loved ones. My mum developed Parkinson's Disease a few years ago. I didn't know anything about the condition at the time, but it's caused by the formation of Lewy Bodies (blobs of abnormally-folded alpha-synuclein protein) in the substantia nigra part of the brain, which controls movement. This part of the brain has high levels of the Vitamin D receptor. Why does the brain contain Vitamin D receptors?
As Lewy Bodies form in other parts of the brain, mental faculties decline. The hippocampus is involved with short-term memory. The neocortex is involved with concious thought.
Mum started showing obvious signs of mental impairment in August 2007. She was assessed by a Community Psychiatric Nurse (CPN) in January 2008 when she scored 14/30 in a MMSE. She was unable to remember 3 words or follow 2 simple instructions in a row (e.g. fold this piece of paper in half and put it on the floor). I started her on 5,000iu/day of Vitamin D3 as it was having a positive effect on my mental function. She was prescribed Aricept, starting at 5mg/day for a month then increasing to 10mg/day. In May 2008 she was re-assessed and scored 26/30 in a MMSE. EDIT: In 2010, Mum's consultant told me that Aricept increases MMSE score by 3 points on average.
Unfortunately, Aricept has side-effects including severe diarrhoea and worsening of the symptoms of Parkinson's Disease which she complained about, so her Aricept dose was reduced back to 5mg/day.
Unsurprisingly, this resulted in a slight decline in mum's mental faculties. In November 2008, I increased her intake of smoked salmon to about 400g/week, as the consumption of long-chain pufas have benefits. See
Low Plasma N-3 Fatty Acids and Dementia in Older Persons: The InCHIANTI Study and
Disruption of glial (oligodendrocyte and astrocyte) cellular function leads to carnosine (b-alanyl-L-histidine) synthesis failure, and nutrient and protective factor deficiency in neurons with secondary development of oxidative stress and amyloid toxicity, with subsequent neuronal dysfunction and development of dementia which stated "Measures which reduce toxicity to vascular endothelium and glia, such as fish oil, may have potential for reducing the likelihood of development of the disease..."
After about four weeks, this had a noticeable (by myself and mum's friend) positive effect on her mental faculties so, inspired by Dr Art Ayers, I started her on Turmeric (curcumin) extract and Goldenseal (berberine) extract. See
Curcumin inhibits aggregation of alpha-synuclein
Neuroprotective effects of curcumin
Alpha-synuclein assembly as a therapeutic target of Parkinson's disease and related disorders
Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model
Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers
Research on the mechanism of neuronal apoptosis in Alzheimer's disease and the effects of tetrohydroberberine on the apoptosis... and
Berberine chloride can ameliorate the spatial memory impairment and increase the expression of interleukin-1beta and inducible nitric oxide synthase in the rat model of Alzheimer's disease.
On January 12th 2009, mum was re-assessed and scored 26/30 in a MMSE. I thought that this was impressive considering that a) she was taking half the dose of Aricept compared to when she previously got that score, b) she had no adverse effects from taking any of the supplements and c) she was 8 months older and degenerative brain diseases worsen with time.
I mentioned to the CPN who did the MMSE that I was starting mum on 15mg/week Vitamin K2 as there were benefits. See
Menaquinone-4 concentration is correlated with sphingolipid concentrations in rat brain ,
Vitamin K status influences brain sulfatide metabolism in young mice and rats ,
Vitamin K and sphingolipid metabolism: evidence to date ,
Substantial sulfatide deficiency and ceramide elevation in very early Alzheimer's disease: potential role in disease pathogenesis and
The possible role of vitamin K deficiency in the pathogenesis of Alzheimer's disease and in augmenting brain damage associated with cardiovascular disease
I don't know what sphingolipids are (I know who probably does) but sulfatides are good and ceramides are bad.
Around the time that mum collapsed, I received a copy of a letter from the CPN to mum's GP which stated "I have informed him (i.e. me) that I am unaware of any robust evidence that these substances are of any benefit." However, there is no evidence that these substances are of any harm.
And finally......
What started the cascade of confusion and collapse leading to hospitalisation and discharge to a nursing home was a simple Urinary Tract Infection (UTI) of e. coli. I don't know why UTIs cause so much confusion in elderly people, but elderly females are at a high risk of developing UTIs because a) elderly people don't drink enough so they don't pass enough urine, b) females have insufficient spacing between anus & urethra and c) elderly females who have any urinary/faecal leakage wear a Tena disposable "nappy/diaper", which increases the likelihood of faeces entering the urethra.
To reduce the risk of further UTIs, I have supplied the nursing home with a pot of D-mannose Plus, which contains d-mannose and cranberry extract, with instructions to add a heaped teaspoonful to a glass of juice once a week. See Intervening with urinary tract infections using anti-adhesives based on the crystal structure of the FimH-oligomannose-3 complex and
Natural approaches to prevention and treatment of infections of the lower urinary tract
EDIT: Thanks to Galina L for bringing the following study to my attention.
Magnesium supplementation in the treatment of dementia patients.
It's probably of no help to Lewy Body Dementia sufferers, as they already have high Mg levels in their CSF. See CSF Mg and Ca as diagnostic markers for dementia with Lewy bodies.
Continued on Look after your brain, Part 2.
Vitamin K
After Vitamin D, Vitamin K will be the "next big thing" you hear about in the media. Why? Just Google "Vitamin K" and see what comes up. At the top of the list is good ol' Wikipedia.
Vitamin K used to be thought of as only the blood clotting vitamin. Some new-borns have to be given Vitamin K injections to ensure proper clotting. However, Vitamin K is needed for the carboxylation of osteocalcin in Bone Matrix Gla Proteins. The what of what in what? In simple terms, Vitamin K is needed to ensure that dietary calcium goes into your bones, rather than into your artery walls, kidneys, brain etc. A lack of Vitamin K can cause osteoporosis. To prevent/treat osteoporosis, either Vitamin K1 (phylloquinone) or Vitamin K2 (menaquinone or menatetrenone) will do.
I used 15mg/day of K2 (plus 1.5g/day of Ca plus 400mg/day of Mg plus ~1,000iu/day of D3) to reverse osteoporosis in my lumbar spine (bone density by DEXA went from -2SD to 0SD) in 3 years.
However, only Vitamin K2 is effective at removing calcium from the media of artery walls. In The Rotterdam Study, "The relative risk (RR) of CHD mortality was reduced in the upper tertile of dietary menaquinone (K2) compared to the lower tertile (RR 0.43, 95% CI: 0.24, 0.77). Phylloquinone (K1) intake was not related to any of the outcomes." An RR of 0.43 means, on average, a 57% reduction in heart attack deaths. I've now put K2 in Cholesterol & Coronary Heart Disease.
Vitamin K2 is required for brain health. See Look after your brain.
Vitamin K2 is required for glucose disposal. See Vitamin K₂ prevents hyperglycemia and cancellous osteopenia in rats with streptozotocin-induced type 1 diabetes and Vitamins D and K as Pleiotropic Nutrients.
Good food sources of Vitamin K2 can be found here.
Warfarin antagonises Vitamin K, so it can result in arterial calcification. Anyone taking warfarin should ask their GP for regular check-ups to keep an eye on this potential problem.
Vitamin K used to be thought of as only the blood clotting vitamin. Some new-borns have to be given Vitamin K injections to ensure proper clotting. However, Vitamin K is needed for the carboxylation of osteocalcin in Bone Matrix Gla Proteins. The what of what in what? In simple terms, Vitamin K is needed to ensure that dietary calcium goes into your bones, rather than into your artery walls, kidneys, brain etc. A lack of Vitamin K can cause osteoporosis. To prevent/treat osteoporosis, either Vitamin K1 (phylloquinone) or Vitamin K2 (menaquinone or menatetrenone) will do.
I used 15mg/day of K2 (plus 1.5g/day of Ca plus 400mg/day of Mg plus ~1,000iu/day of D3) to reverse osteoporosis in my lumbar spine (bone density by DEXA went from -2SD to 0SD) in 3 years.
However, only Vitamin K2 is effective at removing calcium from the media of artery walls. In The Rotterdam Study, "The relative risk (RR) of CHD mortality was reduced in the upper tertile of dietary menaquinone (K2) compared to the lower tertile (RR 0.43, 95% CI: 0.24, 0.77). Phylloquinone (K1) intake was not related to any of the outcomes." An RR of 0.43 means, on average, a 57% reduction in heart attack deaths. I've now put K2 in Cholesterol & Coronary Heart Disease.
Vitamin K2 is required for brain health. See Look after your brain.
Vitamin K2 is required for glucose disposal. See Vitamin K₂ prevents hyperglycemia and cancellous osteopenia in rats with streptozotocin-induced type 1 diabetes and Vitamins D and K as Pleiotropic Nutrients.
Good food sources of Vitamin K2 can be found here.
Warfarin antagonises Vitamin K, so it can result in arterial calcification. Anyone taking warfarin should ask their GP for regular check-ups to keep an eye on this potential problem.