Tuesday, 20 November 2012

Thursday, 1 November 2012

Wednesday, 13 June 2012

August 201 Resources

July 2012 Resources

June 2012 resources

May 2012 Resources

when you eat

senobi stretch and breathe
parasympatheitic self pdf
mawson webcam
Igloo
C difficile diaherra go to earth clinic re fecal transplant
zeo sleep monitor
Ed Dale ituines
UK power breath exercise blower
face mask for power breath
fitbit scales
breathing rate app bought
sleep alarm app
ithoughts mindmap
american crew amazon
amazon nostril blocker
pubmed hypercapnia
hypothalamus inflammation
vagus nerve conttrol of hgh secretion
mri imaging of co2 on brain vessel size
cooling inflammation and menthol
breathing training and vagus nerve
mri renderer of app
muscle app
TNF alpha in smokers inflammtion
Emotional Maltrreatmetn and romantic problems
trans reesveratrol stop malecualr degeneration
Wolverine
hypoxia and cancer in lung
resveratrol suply eye test
GI and bacteria sweden
GI Infections and cancer 1 in 6
Jesse Livermore and Dreyfus
fukushima rss
fullerne supply usa
fullerene suppuniversity
GI and Mast cells
hiccup cure
mice hair and testes
Standford personalised medicaine
Rutin and anti clotting
.longevinex.com/supplementfacts.php
Harvard and Rutin
Parkinson Funding Gene upregualte
MADONNA and gut
Sarah Miles Henry Butt CFShttp://www.drmyhill.co.uk/cfs_book.pdf
Watse to height measure
Omega 3 lab
Lipid doctor USA_01
Parkinsons and K2
second opinion linoeic acid fats
keynes chalrstom usa
Lizard anti addition food
With that knowledge let's get back to the case. This young man with a history of abnormal
cholesterol suddenly developed massive elevations of both cholesterol and TG. Something sure
turned on his lipogenic genes. That something is the fairly acute onset of type 2 diabetes mellitus.
As the lipid levels became grossly pathological, the first manifestation was not the pancreatitis but
rather the deposition of the TG into the dermis causing eruptive xanthomas. Tragically that
diagnosis was missed and that could have had lethal consequences (pancreatitis can be fatal).
When you see rapid onset of papulovesiclular lesions on trunks and extremities, eruptive
xanthomas have to be in the differential diagnosis. They are often quite pruritic. It takes 5 minutes
to make the diagnosis: draw a red top tube, spin it and you will see "milk" not clear yellow serum.
Or pick up and ophthalmoscope and glance at the retina where you might see white rather
than red arterial vessels (lipemia retinalis). Both FA and cholesterol lipogenic genes (influenced
by the nuclear transcription factors (NTF) sterol regulatory element binding proteins (SREBP) 2
and 1C can go crazy when the glycemia onset is sudden in insulin resistant and/or insulin
deficient patients developing T2DM. These NTF or genes cause synthesis of enzymes
(lipogenic) that create lipids: such as DGAT, HMGCoA reductase) The FA are rapidly converted
to TG which utilizing MTP joins lots of newly synthesized FC, and CE forming chylomicra and
VLDLs. As one would expect in someone with extreme hypercholesterolemia and
hypertriglyceridemia, there is a massive increase in large TG-rich lipoproteins as evidenced by
the VLDL-P (147 nmol/L). In this case they are both chylos and VLDLs. One cannot differentiate
between chylomicra and VLDL using NMR -- they are simply both very large TG trafficking
particles and reported as large VLDL-P.
The acute onset of T2DM (due to IR and insulin
It was the change in my own attitude toward the game that was of supreme importance to me. It taught me, little by little, the essential difference between betting on fluctuations and anticipating inevitable advances and declines, between gambling and speculating. I think it was a long step forward in my trading education when I realized at last that when old Mr. Partridge kept on telling the other customers, "Well, you know this is a bull market!" he really meant to tell them that the big money was not in the individual fluctuations but in the main movements that is, not in reading the tape but in sizing up the entire market and its trend. And right here let me say one thing: After spending many years in Wall Street and after making and losing millions of dollars I want to tell you this: It never was my thinking that made the big money for me. It always was my sitting. Got that? My sitting tight! It is no trick at all to be right on the market. You always find lots of early bulls in bull markets and early bears in bear markets. I’ve known many men who were right at exactly the right time, and began buying or selling stocks when prices were at the very level which should show the greatest profit. And their experience invariably matched mine that is, they made no real money out of it. Men who can both be right and sit tight are uncommon. I found it one of the hardest things to learn. But it is only after a stock operator has firmly grasped this that he can make big money. It is literally true that millions come easier to a trader after he knows how to trade than hundreds did in the days of his ignorance. – Jesse Livermore

Wednesday, 9 May 2012

Sunday, 6 May 2012

May 2012 resources

when you eat
senobi stretch and breathe
parasympatheitic self pdf
mawson webcam
Igloo
C difficile diaherra go to earth clinic re fecal transplant
zeo sleep monitor
Ed Dale ituines
UK power breath exercise blower
face mask for power breath
fitbit scales
breathing rate app bought
sleep alarm app
ithoughts mindmap
american crew amazon
amazon nostril blocker
pubmed hypercapnia
hypothalamus inflammation
vagus nerve conttrol of hgh secretion
mri imaging of co2 on brain vessel size
cooling inflammation and menthol
breathing training and vagus nerve
mri renderer of app
muscle app
TNF alpha in smokers inflammtion
Emotional Maltrreatmetn and romantic problems
trans reesveratrol stop malecualr degeneration
Wolverine
hypoxia and cancer in lung
resveratrol suply eye test
GI and bacteria sweden
GI Infections and cancer 1 in 6
Jesse Livermore and Dreyfus
fukushima rss
fullerne supply usa
fullerene suppuniversity
GI and Mast cells
hiccup cure
mice hair and testes
Standford personalised medicaine
Rutin and anti clotting
.longevinex.com/supplementfacts.php
Harvard and Rutin
Parkinson Funding Gene upregualte
MADONNA and gut
Sarah Miles Henry Butt CFShttp://www.drmyhill.co.uk/cfs_book.pdf
Watse to height measure
Omega 3 lab
Lipid doctor USA_01
Parkinsons and K2
second opinion linoeic acid fats
keynes chalrstom usa
Lizard anti addition food
With that knowledge let's get back to the case. This young man with a history of abnormal
cholesterol suddenly developed massive elevations of both cholesterol and TG. Something sure
turned on his lipogenic genes. That something is the fairly acute onset of type 2 diabetes mellitus.
As the lipid levels became grossly pathological, the first manifestation was not the pancreatitis but
rather the deposition of the TG into the dermis causing eruptive xanthomas. Tragically that
diagnosis was missed and that could have had lethal consequences (pancreatitis can be fatal).
When you see rapid onset of papulovesiclular lesions on trunks and extremities, eruptive
xanthomas have to be in the differential diagnosis. They are often quite pruritic. It takes 5 minutes
to make the diagnosis: draw a red top tube, spin it and you will see "milk" not clear yellow serum.
Or pick up and ophthalmoscope and glance at the retina where you might see white rather
than red arterial vessels (lipemia retinalis). Both FA and cholesterol lipogenic genes (influenced
by the nuclear transcription factors (NTF) sterol regulatory element binding proteins (SREBP) 2
and 1C can go crazy when the glycemia onset is sudden in insulin resistant and/or insulin
deficient patients developing T2DM. These NTF or genes cause synthesis of enzymes
(lipogenic) that create lipids: such as DGAT, HMGCoA reductase) The FA are rapidly converted
to TG which utilizing MTP joins lots of newly synthesized FC, and CE forming chylomicra and
VLDLs. As one would expect in someone with extreme hypercholesterolemia and
hypertriglyceridemia, there is a massive increase in large TG-rich lipoproteins as evidenced by
the VLDL-P (147 nmol/L). In this case they are both chylos and VLDLs. One cannot differentiate
between chylomicra and VLDL using NMR -- they are simply both very large TG trafficking
particles and reported as large VLDL-P.
The acute onset of T2DM (due to IR and insulin
It was the change in my own attitude toward the game that was of supreme importance to me. It taught me, little by little, the essential difference between betting on fluctuations and anticipating inevitable advances and declines, between gambling and speculating. I think it was a long step forward in my trading education when I realized at last that when old Mr. Partridge kept on telling the other customers, "Well, you know this is a bull market!" he really meant to tell them that the big money was not in the individual fluctuations but in the main movements that is, not in reading the tape but in sizing up the entire market and its trend. And right here let me say one thing: After spending many years in Wall Street and after making and losing millions of dollars I want to tell you this: It never was my thinking that made the big money for me. It always was my sitting. Got that? My sitting tight! It is no trick at all to be right on the market. You always find lots of early bulls in bull markets and early bears in bear markets. I’ve known many men who were right at exactly the right time, and began buying or selling stocks when prices were at the very level which should show the greatest profit. And their experience invariably matched mine that is, they made no real money out of it. Men who can both be right and sit tight are uncommon. I found it one of the hardest things to learn. But it is only after a stock operator has firmly grasped this that he can make big money. It is literally true that millions come easier to a trader after he knows how to trade than hundreds did in the days of his ignorance. – Jesse Livermore

Friday, 27 April 2012

Brain Items

Russell Blacock video
Lucas Tafur
Repair of brain with plant chemicals
Heart and heart surgeon on statins
Clean asian sauces
microgial inflammation and japanese chemical to down rgulate
why msg and the japanese do not get any effects

Wednesday, 25 April 2012

April 2012 Resources

May 2012

April

In the woo blog
TED on cheating behavioural nursing and economics
Grass fed beef
How vit c works
hoe antidepressants spur brain growth
Argan oil from mirocco
beating cancer with diet
dreid prunes and satiety
Blog, fat burning man, through jack kruse
zeo brain waves during sleep
I3 mindware for memory improvement
Blog through jack kruse
Bill Hnederson healing cancer gently
oyster mushroom and cancer
Sinus washing
WAT to BAT harvard
Russian Breathing knowhow
Scientists research data does not stand up Seths Blog
Lack of repeatability in cancer research Seths Blog
Running, oxygen vo2, depression
food combining for fat cell attack
oxygen demand of 20% and timing during tissue regrowth
Seth blog why scientists need to pay their mortgage too
oxygen russian and cold
Jack Says:
April 24th, 2012 at 10:35 am @Adam
VO2 Max assessment (cardiopulmonary findings lead to a work up if needed.) A VO2 max is now a very easy test to get from many gyms of from trainers. It does not require a physician to order but to get an optimal bio-hack of the data it might. People with cardiovascular disease should seriously consider getting this test done to know what their abilities will be given how much life are left in their lungs and heart. You can also use this bad boy to know how much HIIT you should start with. These are baselines one can use and not set in stone.
Classes: Worse to best directly from the test. Find your class and plug in your Primal exercise routine.
A. VO2 max < 20 ml/kg/min You should walk 15 min 5-7 days per only
B. VO2 max < 20-25 ml/kg/min You should perform 15 minutes of aerobic work 5-7 days a week with one anaerobic interval An anaerobic interval = 0-5 sec
C. VO2 max < 25-30 ml/kg/min You should perform 20 minutes of aerobic activity with 2 anaerobic Intervals 4-5 times a week. An Interval = 5-15 sec
D. VO2 max < 30-35 ml/kg/min You should perform 20 min of HIIT with 4 Intervals 4 times per week where each anaerobic Interval is 5-15 sec.
E. VO2 max < 35-40 ml/kg/min You should perform 20 minutes of HIIT 3 times a week with 4 Intervals where each Interval is 15-30 sec , where recovery is 3-5 sec. You can also add 30 minutes of steady state cardio (sprints) once a week
F. VO2 max 30 sec. Recovery can be 1-2 minutes.
G. VO2 max 45+ ml/kg/min You should perform 20 min of HIIT with 6 Intervals 3 days a week. The Interval is >45 sec and your recovery must be less than 1 minute.

Friday, 6 April 2012

Brain turmor and Ketogenic diet

Metabolic management of glioblastoma multiforme using standard therapy together with a restricted ketogenic diet: Case Report

PubMed Paper

Background

Management of glioblastoma multiforme (GBM) has been difficult using standard therapy (radiation with temozolomide chemotherapy). The ketogenic diet is used commonly to treat refractory epilepsy in children and, when administered in restricted amounts, can also target energy metabolism in brain tumors. We report the case of a 65-year-old woman who presented with progressive memory loss, chronic headaches, nausea, and a right hemisphere multi-centric tumor seen with magnetic resonance imaging (MRI). Following incomplete surgical resection, the patient was diagnosed with glioblastoma multiforme expressing hypermethylation of the MGMT gene promoter.

Methods

Prior to initiation of the standard therapy, the patient conducted water-only therapeutic fasting and a restricted 4:1 (fat: carbohydrate + protein) ketogenic diet that delivered about 600 kcal/day. The patient also received the restricted ketogenic diet concomitantly during the standard treatment period. The diet was supplemented with vitamins and minerals. Steroid medication (dexamethasone) was removed during the course of the treatment. The patient was followed using MRI and positron emission tomography with fluoro-deoxy-glucose (FDG-PET).

Results

After two months treatment, the patient's body weight was reduced by about 20% and no discernable brain tumor tissue was detected using either FDG-PET or MRI imaging. Biomarker changes showed reduced levels of blood glucose and elevated levels of urinary ketones. MRI evidence of tumor recurrence was found 10 weeks after suspension of strict diet therapy.

Conclusion

This is the first report of confirmed GBM treated with standard therapy together with a restricted ketogenic diet. As rapid regression of GBM is rare in older patients following incomplete surgical resection and standard therapy alone, the response observed in this case could result in part from the action of the calorie restricted ketogenic diet. Further studies are needed to evaluate the efficacy of restricted ketogenic diets, administered alone or together with standard treatment, as a therapy for GBM and possibly other malignant brain tumors.

Wednesday, 4 April 2012

Parkinsons Melb Uni

White Laboratory

Contact:	Associate Professor Anthony White
Phone:	+61 3 8344 1805
Fax:	+61 3 8344 4004
Email:	arwhite@unimelb.edu.au

The White laboratory studies the role of biometals such as copper (Cu), zinc (Zn) and iron (Fe) in neurodegenerative diseases. These metals have important roles in normal cell functions. However, abnormal biometal metabolism is central to a number of neurodegenerative illnesses including Alzheimer's disease, Parkinson's disease, motor neuron disease and prion disorders. Recent studies have shown that pharmacological modulation of biometal homeostasis in the brain may offer a novel therapeutic approach to treating these brain diseases. An important step in developing these novel drugs is to obtain a clear understanding of how biometals affect neuronal metabolism and synaptic function. Our laboratory is investigating the role of biometals in neuronal cell signaling pathways. We are also developing and testing novel neuroprotective metallo-complexes that may restore brain function in neurodegenerative diseases.

Key research areas are:

Investigating how biometals control neuronal cell signaling pathways

Biometals are central to the pathology of many brain diseases, however, little is known about the normal function of metals such as Cu and Zn in neuronal cell signaling pathways. These pathways affect neuronal survival and synaptic function and are important targets for therapeutic intervention in neurodegeneration. It is critical to obtain a greater understanding of how biometals modulate cell signaling during normal brain function and in disease. We are currently investigating how Cu and Zn control a number of different cell signaling pathways including PI3K, GSK3 and MAPK pathways and how age-related changes to these pathways contribute to neurodegenerative diseases.

Development of neuroprotective metallo-complexes Together with collaborators at the Department of Pathology and Bio21 Institute, we have identified a class of neuroprotective cell permeable metallo-complexes (bis(thiosemicarbazonato)-metal complexes or BTSCs). These small molecules cross the blood brain barrier and enter neurons and glia. Delivery of small levels of Cu or Zn can be modulated by structural changes to the complexes. These metallo-compounds offer exciting potential as a novel therapeutic strategy for treating neurodegenerative diseases. Release of the metals activates neuroprotective signaling cascades resulting in significant improvements in multiple animal models of neurodegeneration including Alzheimer’s disease, Parkinson’s disease and motor neuron disease. We are currently using cell culture and animal models to investigate the uptake, metal release and activation of neuroprotective pathways of these important compounds with the aim of moving the compounds into pre-clinical testing for treatment of neurodegeneration.
This project was identified by the National Health and Medical Research Council of Australia (NH&MRC) as one of the Top Ten Research Projects funded in 2010. http://www.nhmrc.gov.au/guidelines/publications/r48

Ther release

Potential Strategy To Restore Motor And Cognitive Function In Parkinson's Disease

Main Category: Parkinson's Disease
Also Included In: Radiology / Nuclear Medicine
Article Date: 04 Apr 2012 - 1:00 PDT

An agent under consideration for use in PET imaging combats neuronal death to relieve Parkinsonian symptoms in animal models, according to a study published in the Journal of Experimental Medicine.

The movement-related symptoms of Parkinson's disease, including muscle rigidity and tremors, are caused by the loss of dopamine-secreting neurons in the brain. Current therapies aim at increasing and maintaining dopamine levels to correct these motor impairments. However, these approaches do not address the underlying neuronal death that initiated the disease.

David Finkelstein, Kevin Barnham, and colleagues at the University of Melbourne find that the PET imaging agent CuII(atsm) reverses the neurotoxicity that destroys dopamine-secreting neurons. Improvements in motor skills and memory were observed after treatment in four unique animal models of Parkinson's disease. The authors suggest this compound functions as a scavenger of peroxynitrite, whose accumulation is known to promote neuronal death.

These results point to a potential strategy to restore motor and cognitive function in Parkinson's disease patients by reviving neuronal function rather than solely masking symptoms.

Tuesday, 3 April 2012

Vitamin B12 norman swan

fenech B12 folate levels

telomere

http://www.abc.net.au/radionational/programs/healthreport/vitamin-b12-supplementation/3823160

Vitamin B12 supplementation

Broadcast:: Monday 13 February 2012 5:42PM (view full episode)

A neurologist from the University of Western Ontario in Canada argues the case for vitamin B12 supplementation for the brain and heart.

View comments (22)

Transcript

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Norman Swan: Now to that vitamin B12 story I promised you earlier. One risk factor for heart attacks, strokes and dementia is a substance in the blood called homocysteine. It’s enormously controversial as you’ll hear but in a recent editorial in the Journal of the American Medical Association (JAMA) -- David Spence, who’s Professor of Neurology and Clinical Pharmacology at the University of Western Ontario in Canada, argued that there’s more to homocysteine lowering than many doctors think -- but it’s how you do it.
David Spence: Homocysteine is very clearly a risk factor. In the animal studies it’s causal of atherosclerosis. The big discrepancy has been between the observational studies, the experimental research in animals and the failure of the clinical trials to show any benefit of vitamin therapy to lower levels of homocysteine.
Norman Swan: And the fact is that the vitamins such as folate B6 and B12 do lower homocysteine, but the lowering doesn’t seem to flow through at least to coronary heart disease and dementia.
David Spence: Well actually no, there is pretty good evidence from Holland and the UK that vitamin therapy does improve dementia. The VITACOG studies by Helga Refsum and David Smith at Oxford do show improvements in dementia and a reduction of brain shrinkage on MRI, but the studies did not show what everybody expected which was a reduction of myocardial infarction and in fact it’s much more complicated than everybody thought. So there is a trial from McMaster University in Canada called the HOPE-2 Study. That was the first study to use a decent dose of vitamin B12. They used a milligram of B12, that’s 1,000 micrograms a day, which is the dose that is needed for elderly people with relatively poor absorption of B12. In the HOPE-2 Study the 1,000 micrograms of B12 along with folic acid and B6 significantly reduced strokes by 23%. But the authors, being cardiologists and therefore innocent of the circulation of the brain, they literally said ‘well we couldn’t think of a biological difference between heart attacks and strokes, so we concluded that this was a chance finding’.
Norman Swan: And the reason they said that was that the claim is that strokes occur because you get a clot, atherosclerosis in the artery in your neck, your carotid artery, which then breaks off and lodges in the brain which is analogous to what happens in a heart artery to get a heart attack or a myocardial infarction.
David Spence: Yes but it’s different. Virtually all heart attacks are caused by an occlusion of a coronary artery. A plaque ruptures, the artery occludes, a clot forms that causes a heart attack. Most strokes on the other hand are caused by emboli to the brain, so chunks of plaque or clots break off from the heart or the arteries and they get thrown up into the brain arteries by the circulation of the blood.
And a high level of homocysteine, which is a clotting factor, more than quadruples the risk of stroke in patients who have a heart rhythm the surgeons called atrial fibrillation, because homocysteine is a clotting factor, so heart attacks and strokes are not the same and it shouldn’t have been a surprise really that strokes were prevented when heart attacks weren’t. What’s transpired in the last several years is the juxtaposition of two studies that we did that have made it apparent that things were much more complicated than we thought.
So in 2005 we published a paper about a sub-group analysis of the VISP trial, vitamin intervention for stroke prevention trial.
Norman Swan: And just to explain: When you talk about sub-group analysis some epidemiologists raise the sign of the cross when people say sub-group analysis. This means that you’ve taken a group of people within the study with particular characteristics and said this is what happens to them. It might not happen to everybody else but this is what happens to them and the critics say you should never do sub-group analysis, in fact we’ve had them on the Health Report because you didn’t design it for sub-groups to begin with and you’ve got no idea whether it’s a real finding or not.
David Spence: Yeah, that’s a very popular approach. The recent commentary that we wrote in the JAMA points out that sub-group analysis can be very informative.
Norman Swan: It gets pretty detailed but it’s worth listening because given the huge volume of vitamin supplements that Australians consume each year, David Spence’s work shows how the effects of vitamins differ hugely depending on our individual circumstances.
For example the VISP trial to prevent stroke failed to show an effect of B vitamins. David Spence believes that’s because folate was added to the flour supply around that time which meant people weren’t folic acid deficient. And the researchers also made the mistake of giving people who were B12 deficient vitamin B12 no matter whether they were in the placebo or treatment group.
David Spence: So we said let’s look at what happens if we exclude these people who got the B12 injections and while we’re at it we’ll also exclude the people who had kidney failure. The reason we did that wasn’t for what turned out to be probably the right reasons, we excluded them because we thought they would not respond to vitamin therapy. So in this sub-group analysis we had about two thirds of the patients from the VISP trial and in that group we showed a very significant reduction of strokes, heart attacks and death, there was a 34% reduction in strokes, heart attacks and death.
Norman Swan: So this is between those who had high vitamin B12 versus those who had low?
David Spence: Yes, that study suggested that vitamin B12 is probably pretty important in all this and we never realised that excluding the renal failure was the key to the benefits. So we published last year in JAMA a study in patients with diabetic kidney problems and we used a higher dose of B12 than we used in the VISP and we randomised these patients who had diabetic kidney disease to high dose vitamins versus placebo and when we got the results I was completely gobsmacked.
I thought we must have reversed the randomisation code because the high dose vitamins actually made things worse. The kidney function declined more quickly and they were twice as likely to have cardiovascular events, so death, myocardial infarctions, stroke, progression to dialysis and amputation, those were all combined. This meant that in patients with kidney failure the vitamins made things worse, so on the one hand in the VISP sub-group analysis where we excluded patients with kidney failure vitamins it made things better, but in patients with kidney failure vitamins made things worse.
Norman Swan: I apologise if this is making you go cross eyed but it’s really important stuff. You see to go back to the beginning of this story it’s still about homocysteine levels and the risk of blood clots and artery damage. It’s just that in a country like Canada or Australia where we have folic acid in flour, vitamin B12 becomes the main way to bring homocysteine down. And if David Spence is right the kind of vitamin B12 you take is critical.
David Spence: But it’s not just quite that simple. It’s also another factor called ADMA, asymmetric dimethylarginine, and it depends on which B vitamin. The B vitamin that’s harmful is high dose folic acid which increases the blood levels of this antagonist of the good stuff called nitric oxide which is increased in people who have high doses of folic acid and poor kidney function. And on the other hand the vitamin B12 that was used in all these trials was the usual form which is called cyanocobalamin, which has cyanide in it and it turns out that some work in Japan had shown about ten years ago that it if you give cyanocobalamin to patients with kidney failure they get a build up of cyanide and cyanide consumes a factor that is good for the arteries called hydrogen sulphide. And resarchers showed that if you give a different form of B12 called methylcyanocobalamin, not only does it lower the levels of homocysteine but it also lowers the levels of asymmetric dimethylarginine, ADMA. You probably need to be using methylcobalamin in people with impaired kidney function, whereas in the VISP sub-group analysis we showed that ordinary B12 was beneficial when we excluded people with renal failure.
Norman Swan: So somebody is listening to us now to a very complicated story and a very important story, but a complicated story, how does that translate to what general practitioners, what consumers should be doing if they think well, should I be having my homocysteine level measured, should I be having my B12, what in fact is the right dose of vitamin B12, because you in your papers have argued that in fact what people are recommended as supplementation is probably really not adequate. Can you summarise what the consumer’s story is here?
David Spence: Yes, so vitamin B12 deficiency is very common and missed much of the time.
Norman Swan: Why is it so common because when I was at medical school we were told the cause of low vitamin B12 is a condition called pernicious anaemia which is like an auto immune disease attacking the stomach and the stomach fails to absorb it from the diet.
David Spence: Yes that’s an intrinsic factor and that’s only one of the six ways that B12 can go wrong. B12 absorption is extraordinarily complex, to absorb B12 you need haptocorrin from saliva, you need stomach acid, you need intrinsic factor, you need pancreatic third factor...
Norman Swan: And what you’re describing here are chemicals that are excreted by different parts of the intestinal tract, the stomach, the mouth and the pancreas which help chemically to absorb vitamin B12 from the bowel.
David Spence: Yes, there are about six ways for B12 absorption to go wrong and it turns out that when you measure serum B12 it does not do a good job of detecting the B12 deficiency, because only something between 6% and 20% of serum B12 is active. So in order to know if someone has metabolic B12 deficiency you have to measure either methylmalonic acid, which is hard to get done, or in people who are folate deplete you can measure homocysteine and it turns out when you do that the serum B12 below, either methylmalonic acid or homocysteine which begins to rise is 400 picomoles per litre and the normal range is from 160 to 600. So almost two thirds of the people in that normal range could have functional B12 deficiency and in order to know whether they do or don’t you have to measure either their methylmalonic acid or homocysteine. And when you do that, metabolic B12 deficiency in my patients with vascular disease is present in 12% of those below age 50 and 13% of those between age 50 and 71 and 30% of patients above age 71. So it’s very, very common and it’s really important because B12 deficiency not only raises the levels of homocysteine, increases clotting of the blood, increases deep vein thrombosis, quadruples the risk of stroke and atrial fibrillation but B12 deficiency also causes damage to the peripheral nerves, the spinal cord and dementia. And so that’s why Helga Refsum and David Smith at Oxford have shown that even in the normal range you can have shrinkage of the brain and dementia with B12 deficiency with normal serum B12 levels.
Norman Swan: So what’s the practical, I mean this is very complicated and time consuming for a busy general practitioner to take on, is it such that you would almost put it in the water supply. I mean what’s the story here?
David Spence: Well not cyannacobalamin.
Norman Swan: But you know what I’m saying here, what’s the public health message here does everybody get it?
David Spence: Well the public health message is that vitamin B12 deficiency is way commoner than everybody thinks and in order to know if someone has B12 deficiency you can’t just measure a serum B12. In Europe they measure something called holotranscobalamin, not readily available here and probably not in Australia. So if you have somebody who has a borderline B12 level you’ve got to measure the homocysteine level to know whether they have metabolic B12 deficiency.
Norman Swan: So that’s after they’ve been fully replaced with folate, otherwise you don’t know where you are?
David Spence: Yeah, so over here that’s not an issue because we have folic acid fortification of the grain supply so we don’t have folate deficiency anymore.
Norman Swan: Then the question becomes how -- you’ve already discussed the two forms of vitamin B12, but if you’ve got a problem absorbing it, I mean if you’ve got pernicious anaemia and you’ve lost this intrinsic factor as they call it from the stomach they say give vitamin B12 injections, don’t swallow it because you’re not going to absorb it.
David Spence: Most people don’t need injections except maybe at the beginning so what’s going on is that you need vitamin B12 for DNA synthesis, so the cells that get in trouble when you have a shortage of B12 are the cells that turn over quickly so we get anaemia because red cells turn over in 100 days, you get low platelet counts because platelets turn over in 10 days. And it turns out that the intestinal villi turn over in three days, so one of the things that happens in deficiency of either folate or B12 is that the intestinal villi shrivel and then you lose a huge amount of the surface area of the intestine and you become unable to absorb B12.
Norman Swan: It’s a vicious cycle
David Spence: Yes, so some people need injections of B12 in the beginning to restore the intestinal villi and then they can absorb oral B12. And the doses that are used are way bigger than the recommended daily intake for people with normal absorption so you can absorb enough B12 from oral B12 by mass transfer without the intrinsic factor but that’s when you’re getting up to these doses of 1,000 micrograms a day.
Norman Swan: Somebody is listening to this and they are 60 years old with no heart disease, feeling fine, good diet, do they go along to the GP and ask for a vitamin B12 level?
David Spence: Yes they should also have a TSH level to see if they have hypo-thryoidism.
Norman Swan: And if a GP is listening to this and has got somebody in front of them with the beginnings of heart disease you would argue they need a vitamin B12 level because that’s the high risk group for vitamin B12 deficiency.
David Spence: Yeah, and homocysteine quadruples the risk of stroke and atrial fibrillation.
Norman Swan: And homocysteine is probably the best way of measuring it really in practical terms. How do you know whether or not they need an injection?
David Spence: What I usually go by is if the B12 level is very low, you know below 150 or something like that then they are probably going to need injections. You can sort it out by giving them oral vitamin B12 repeating the blood level in a month and seeing if it’s come up above 400 and if it hasn’t they might need injections.
Norman Swan: And putting your hand on your heart you feel the randomised control trial evidence is strong enough to recommend this course of action on a mass scale?
David Spence: Well the HOPE-2 trial and the VISP sub-group analysis yeah, I think so.
Norman Swan: There’s a statistic in epidemiology called population attributable risk, and this is really saying look, if you take everybody who’s had a stroke, or everybody who gets a stroke in a year, what percentage of those strokes could be blamed on low B12 and high homocysteine?
David Spence: Yes, so it’s all related to age so if you take the attributable risk of stroke from atrial fibrillation, which is tightly connected to homocysteine I think, at age 50 only one and a half percent of strokes are due to atrial fibrillation.
Norman Swan: This is where the top two chambers of the heart kind of quiver, don’t beat properly and you often get a little pouch growing off the left atrium which collects a clot which can then break off and lodge in the brain.
David Spence: Yeah and that causes one and a half percent of strokes at age 50, but it causes almost a quarter of strokes at age 80 and the homocysteine is a big factor in the older people. So I published in the Lancet a couple of years ago a nice graph showing that homocysteine levels above 14 which are reckoned to be a clotting factor are only present in about 10% of patients at age 30, but it’s 40% of my patients at age 80. So I think that at the older age groups homocysteine accounts for a substantial proportion of strokes.
Norman Swan: Inevitably people will say ‘oh, I don’t like taking supplements can’t I do this from my diet, can’t I get the vitamin B12 from my diet’?
David Spence: No, vitamin B12 comes from meat and meat is bad for you.
Norman Swan: And you’ve got to eat too much of it?
David Spence: Yes.
Norman Swan: David Spence is Professor of Neurology at Clinical Pharmacology at the University of Western Ontario in Canada.
References:
Spence JD and Stampfer MJ Understanding the Complexity of Homocysteine Lowering With Vitamins. (Commentary) JAMA, December 21, 2011;306;23:2610-2611
House AA et al. Effect of B-Vitamin Therapy on Progression of Diabetic Nephropathy. A Randomized Controlled Trial. JAMA, April 28, 2010;303;16:1603-1609
J. David Spence Atrial fibrillation, stroke prevention therapy and aging. News & Views. Nature, July 2009;6:1-2
Spence JD. Homocysteine-lowering therapy: a role in stroke prevention? Lancet Neurology 2007;7:830-8
Spence JD et al. Vitamin Intervention for Stroke Prevention Trial: an efficacy analysis. Stroke, 2005;36:2404-9
The Heart Outcomes Prevention Evaluation (HOPE) 2 investigators. Homocysteine Lowering with Folic Acid and B Vitamins in Vascular Disease. New England Journal of Medicine 2006;354:1567-1577
Spence JD et al. Vitamin Intervention for Stroke Prevention (VISP) trial: rationale and design. Neuroepidemiology 2001, Feb. 20(1):16-25

Guests

Professor David Spence: Professor of Neurology and Clinical Pharmacology,
University of Western Ontario,
Canada

Sunday, 1 April 2012

from earth clinic

experiment: test this remedy on scalp which has some similarities to cradle cap
April 2nd 345pm
scalp stings
leave it on for 15 minutes

BAKING SODA PASTE

Ratings:

YEA

[YEA] 05/28/2009: Melinda from Ballarat, Victoria, Australia: "This one has been in my family for decades. Want to see instant results? It's wonderful. To get rid of cradle cap simply mix together 2 tablespoons of bi-carb soda with enough water to make a thick paste. About 40 mls of water. Gently rub the paste in to the baby's scalp for a minute and rinse off with warm water. Once a day.The cradle cap usually disappears completely within a few days. Try it, it works."

Replies

[YEA] 10/31/2009: Jessicab from Lorton, Va replies: "WoW!! Thank you for the suggestion of using Bi-carb soda (Baking Soda) and water to make a paste for my baby's cradle cap. I've been alternating with olive oil one day and apple cider vinegar the next. It was working..but very very slowly. I tried the Bi-carb soda paste last night. Made the paste, slathered and rubbed in to daughter's scalp about 20 minutes before bath. I rinsed it out, took a VERY SOFT baby brush and did circular motions around head and then proceeded to wash her head with baby shampoo, rinsed with warm water and WOW what a huge difference. 90% of the cradle cap is gone! I will do it again in a couple of days. I believe you said it typically takes a few doses to cure. Excellent tip..thanks again!"

Arthritis

http://www.lef.org/news/LefDailyNews.htm?NewsID=12605&Section=Nutrition

Her Arthritis Was Cured... with Honey And Vinegar

CATHERINE VONLEDEBUR
Coventry Telegraph
03-27-12

MARGARET Hills was a carefree trainee nurse in 1940s London when she was first diagnosed with arthritis at 22-years-old.
She was in extreme pain and ordered complete bed rest for four months after a Harley Street consultant told her she had a "very enlarged heart".
The eldest of seven children from Lixnaw in County Kerry, had to give up her three favourite pastimes: dancing, cycling and swimming.
Before leaving St Stephen's Hospital in Fulham the Medical Superintendent told her she must never dance, cycle or run uphill again, give up her nurse's training AND never have children.
Margaret thought to herself: "If I am to live my life like this, I may as well be dead."
She ignored the advice and finished her nurse's training in London, got married, moved to Coventry and had eight children - five sons and three daughters.
But for 16 years she continued to suffer from chronic osteo- arthritis and rheumatoid arthritis - in every joint.
At its worst Margaret was taking 12 aspirins a day and wearing a surgical collar, surgical corset and splints on her fingers.
She set out to research a cure and read all the 'natural cure' books she could find until she hit upon the treatment aged 36 that cured her of all signs of arthritis and kept her totally pain-free.
MARGARET'S' best-selling book came about after she wrote a letter about her cider vinegar cure to the Coventry Evening Telegraph in 1982.
In a 1994 interview, Margaret said: "It was a twist of fate which led me to open my clinic."
Her daughter Christine Horner, aged 58, a nutritional therapist, recalls how the letter came about. The mother-of-two said: "My mum read an article in the Coventry Evening Telegraph about the amount of money spent on drugs for arthritic diseases.
"She thought, 'this is ridiculous - what a waste!' and wrote a letter to the paper.
"She described how people could help themselves, she said it was not difficult, she had done it.
"Her life was about to change. The next day the postman delivered sacks of mail and the paper's switchboard was jammed with callers about her letter. The local response was amazing."
On June 16, a follow-up story reported how Margaret was inundated with more than 1,000 enquiries from across the country.
Christine said: "My mother printed out her treatment in the paper and it brought even more letters. Within a matter of weeks she decided to write a book.
"As well as looking after four children and her day job as a district nurse she was up at 3am to write."
The book was originally called Curing Arthritis - The Drug-free Way.
Christine continued: "She found an agent in the area who said: 'It's very difficult to get a book published'.
"But every publisher she approached wanted to publish it.
"As Margaret was a Catholic, she chose the most Christian. It was a best-seller for them, and I updated it in 2004.
"At first people kept coming in to our home in Gibbet Hill, Coventry.
"After work mum would find people waiting for her to get some advice so she set up a clinic at home charging a small fee which was donated to her favourite charity, Baby Lifeline.
"It was set up by Judy Ledger, who my parents fostered when she was 15 years old."
Margaret gave up nursing to focus on her arthritis clinic which later moved to Oaks Precinct, Caesar Road, Kenilworth.
In September 1988 she also opened the Margaret Hills Health Food Shop in Millar Court, Kenilworth.
Margaret wrote: "... day after day the letters arrive from people in various countries telling me how much they have benefitted from following the treatment... and thanking me... I feel so humble and grateful."
One young woman even flew over from Sydney, Australia with her mother hoping for an appointment.
Margaret also did talks - her last was in her home town in Ireland where 900 people gathered.
"There were so many I had to give two talks," laughed Margaret in an interview on November 25 1994.
Margaret died peacefully at her Kenilworth home, aged 78, in May 2003.
Treating Arthritis - The Drugfree Way is currently translated into six languages - Portuguese, Polish, Italian, Romanian, Finnish and Arabic.
Since the family-run Margaret Hills' Clinic opened 30 years ago it has helped thousands.
Christine Horner - the second eldest of Margaret's eight children - and her daughter, Julia Davies, continue Margaret's work.
They are both nutritional therapists and run a pain relief clinic. Christine said: "We treat around 900 people at any given time these days, with the vast majority treated at a distance - by email, phone and post. We also carry out ten to 20 face-to-face consultations and treatments weekly."
The mum-and-daughter team has received hundreds of grateful letters.
In the hallway of the clinic is a map of the world with pins in all the countries where they have patients including Peru, Nigeria, Saudi Arabia, Tibet, Australia, the Falklands and Jamaica.
A consultation is pounds 66.50. For more information, call 01926 854783 or visit www.margarethillsclinic.com

Tuesday, 27 March 2012

gut flora

antibiotics destroy got microflora
starch is need for Klebia for arthritis

Thursday, 22 March 2012

Bones

the telepgragh article
the best iherb equivalent

and here is the telie description
Judith Brodie, chief executive of Arthritis Care, said: “Many people with osteoarthritis live for years in great pain before eventually needing joint replacements. This is the first study to show benefit from strontium ranelate so it is early days, but if there is a treatment which can hold back the disease, delay knee replacements and help people to live more active lives for longer, then it will be good news for the millions of people in the UK with this debilitating condition.”

seaweed bread

Sleep Experiment 01

Date March 23rd, 2012

Goal : Improve Certain Brain Factors: Start with

Melatonin, Cortisol , Autophagy,
Circadian Clock reset and resilience,
up-regulate good receptors, down-regulate "bad receptors"
plus unknown
telomere length
general brain volume, rewiring through neuro-plasticity and health

hypothesis development:

that sleep is a medicine
that sleep is a free medicine
that perfect sleep is a free potent secret medicine
that perfect sleep is a free potent secret medicine as it permits restoration of ancient neuron behavior to an optimal set point where circadian cycle of dark-light worked in ancient times when there was no artificial light pollution and EMF pollution. we go back to blue green algae, and consider the genetic links to humans

background:
resources
computer colour http://stereopsis.com/flux/
room lights

Materials and methods :

Pre sleep,

starts at dusk
apply http://stereopsis.com/flux/ to computer to match spectral light from screen to night
switch on night lighting
prepare for sleep at 1030pm: checklist

sleep phase: no blue light, no photons if possible, cool temperature

bed at 1100pm
exogenous supports : checklist
Jelly lamp for winddown
Hibermate eye shield
bathroom light yellow
jelly wash lamp for wake up

awake phase : measure and note

results:
measure wake up time
measure feeling
measure skin, tiredness of eyes
measure cortisol during day , saliva
measure temperature
measure pulse rate
record fast time
Discussion:
COnclusion

Monday, 5 March 2012

Big Questions

is there a best angle to avoid exogenous hormone therapy? maybe, test
if mainstream does not have the answers, where do i start? Look at the everyday as a mystery.
sleep
the gut

NY TIMES_ Blue Light 2012

http://www.nytimes.com/2012/02/21/health/aging-of-eyes-is-blamed-in-circadian-rhythm-disturbances.html?_r=1

Aging of Eyes Is Blamed for Range of Health Woes

By LAURIE TARKAN

Published: February 20, 2012

THE HYPOTHESIS

Enlarge This Image

Ellen Weinstein

The aging eye filters out blue light, affecting circadian rhythm and health in older adults.

THE INVESTIGATORS

Dr. Martin Mainster and Dr. Patricia Turner, University of Kansas School of Medicine.

For decades, scientists have looked for explanations as to why certain conditions occur with age, among them memory loss, slower reaction time, insomnia and even depression. They have scrupulously investigated such suspects as high cholesterol, obesity, heart disease and an inactive lifestyle.

Now a fascinating body of research supports a largely unrecognized culprit: the aging of the eye.

The gradual yellowing of the lens and the narrowing of the pupil that occur with age disturb the body’s circadian rhythm, contributing to a range of health problems, these studies suggest. As the eyes age, less and less sunlight gets through the lens to reach key cells in the retina that regulate the body’s circadian rhythm, its internal clock.

“We believe the effect is huge and that it’s just beginning to be recognized as a problem,” said Dr. Patricia Turner, an ophthalmologist in Leawood, Kan., who with her husband, Dr. Martin Mainster, a professor of ophthalmology at the University of Kansas Medical School, has written extensively about the effects of the aging eye on health.

Circadian rhythms are the cyclical hormonal and physiological processes that rally the body in the morning to tackle the day’s demands and slow it down at night, allowing the body to rest and repair. This internal clock relies on light to function properly, and studies have found that people whose circadian rhythms are out of sync, like shift workers, are at greater risk for a number of ailments, including insomnia, heart disease and cancer.

“Evolution has built this beautiful timekeeping mechanism, but the clock is not absolutely perfect and needs to be nudged every day,” said Dr. David Berson, whose lab at Brown University studies how the eye communicates with the brain.

So-called photoreceptive cells in the retina absorb sunlight and transmit messages to a part of the brain called the suprachiasmatic nucleus (S.C.N.), which governs the internal clock. The S.C.N. adjusts the body to the environment by initiating the release of the hormone melatonin in the evening and cortisol in the morning.

Melatonin is thought to have many health-promoting functions, and studies have shown that people with low melatonin secretion, a marker for a dysfunctional S.C.N., have a higher incidence of many illnesses, including cancer, diabetes and heart disease.

It was not until 2002 that the eye’s role in synchronizing the circadian rhythm became clear. It was always believed that the well-known rods and cones, which provide conscious vision, were the eye’s only photoreceptors. But Dr. Berson’s team discovered that cells in the inner retina, called retinal ganglion cells, also had photoreceptors and that these cells communicated more directly with the brain.

These vital cells, it turns out, are especially responsive to the blue part of the light spectrum. Among other implications, that discovery has raised questions about our exposure to energy-efficient light bulbs and electronic gadgets, which largely emit blue light.

But blue light also is the part of the spectrum filtered by the eye’s aging lens. In a study published in The British Journal of Ophthalmology, Dr. Mainster and Dr. Turner estimated that by age 45, the photoreceptors of the average adult receive just 50 percent of the light needed to fully stimulate the circadian system. By age 55, it dips to 37 percent, and by age 75, to a mere 17 percent.

“Anything that affects the intensity of light or the wavelength can have important consequences for the synchronization of the circadian rhythm, and that can have effects on all types of physiological processes,” Dr. Berson said.

Several studies, most in European countries, have shown that the effects are not just theoretical. One study, published in the journal Experimental Gerontology, compared how quickly exposure to bright light suppresses melatonin in women in their 20s versus in women in their 50s. The amount of blue light that significantly suppressed melatonin in the younger women had absolutely no effect on melatonin in the older women. “What that shows us is that the same amount of light that makes a young person sit up in the morning, feel awake, have better memory retention and be in a better mood has no effect on older people,” Dr. Turner said.

Another study, published in The Journal of Biological Rhythms, found that after exposure to blue light, younger subjects had increased alertness, decreased sleepiness and improved mood, whereas older subjects felt none of these effects.

Researchers in Sweden studied patients who had cataract surgery to remove their clouded lenses and implant clear intraocular lenses. They found that the incidence of insomnia and daytime sleepiness was significantly reduced. Another study found improved reaction time after cataract surgery.

“We believe that it will eventually be shown that cataract surgery results in higher levels of melatonin, and those people will be less likely to have health problems like cancer and heart disease,” Dr. Turner said.

That is why Dr. Mainster and Dr. Turner question a practice common in cataract surgery. About one-third of the intraocular lenses implanted worldwide are blue-blocking lenses, intended to reduce the risk of macular degeneration by limiting exposure to potentially damaging light.

But there is no good evidence showing that people who have cataract surgery are at greater risk of macular degeneration. And evidence of the body’s need for blue light is increasing, some experts say.

“You can always wear sunglasses if you’re in a brilliant environment that’s uncomfortable. You can remove those sunglasses for optimal circadian function, but you can’t take out the filters if they’re permanently implanted in your eyes,” Dr. Mainster said.

Because of these light-filtering changes, Dr. Mainster and Dr. Turner believe that with age, people should make an effort to expose themselves to bright sunlight or bright indoor lighting when they cannot get outdoors. Older adults are at particular risk, because they spend more time indoors.

“In modern society, most of the time we live in a controlled environment under artificial lights, which are 1,000 to 10,000 times dimmer than sunlight and the wrong part of the spectrum,” Dr. Turner said.

In their own offices, Dr. Mainster and Dr. Turner have installed skylights and extra fluorescent lights to help offset the aging of their own eyes.