Sunday, August 11, 2019

CANADA, BRITAIN, NORWAY: SINGLE PAYER SYSTEM IS DISASTROUS

Rely on preventative medicine, meaning your anti-aging nutritional compounds.  

Vitamin D for headaches and restless leg syndrome, and traumas.  

Vitamin C, not aspirin, for headaches.  Vitamin C strengthens capillaries, rebuilds collagen for blood vessel repair and overall immunity.  

Zinc to help regrow the Thymus gland to its original size.  

Magnesium is important as a co-factor for all other nutrients.  It's an excellent muscle relaxer and nerve tonic.  Key to the effective use of magnesium is absorption.  Make sure you're getting enough.  You'll need more than 105mgs per day. See the bottom of this page.

Allithiamine, which crosses the blood-brain barrier where benfotiamine does not [though still protects against Alzheimer's disease], to protect your autonomic nervous system.  Magnesium and zinc help to make Allithiamine more absorbable.  Dr. Derrick Lonsdale writes that
It is hypothesized that the massive consumption of empty calories, particularly those derived from carbohydrate and fat, results in a high calorie/thiamine ratio as a major cause of disease. Because mild to moderate TD results in pseudo hypoxia in the limbic system and brainstem, emotional and stress reflexes of the autonomic nervous system are stimulated and exaggerated, producing symptoms often diagnosed as psychosomatic disease. If the biochemical lesion is recognized at this stage, the symptoms are easily reversible. If not, and the malnutrition continues, neurodegeneration follows and results in a variety of chronic brain diseases. Results from acceptance of the hypothesis could be tested by performing erythrocyte transketolase tests to pick out those with TD and supplementing the affected individuals with the appropriate dietary supplements.   
Read more by Derrick Lonsdale here

Hyaluronic Acid for joints, spine, eyes, and mobility.

Friday, August 9, 2019

[MAJOR] SURGERY AGES THE BRAIN BY 4 MONTHS & 3 DAYS; STROKE AGES THE BRAIN BY 13 YEARS

BE SURE TO READ THE UPDATE AT THE BOTTOM WHERE SOLUTIONS TO THE PROBLEMS OF COGNITIVE IMPAIRMENT THAT RESULT FROM SURGERY CAN BE HAD.
Yesterday, Drudge linked an article published in Britain's Daily Telegraph titled "Major Surgery Doubles Risk of Substantial Brain Decline, Study Says."  So what did the article say?  
Reading health articles, one must try to be objective.  NOT.  Being objective means to leave your own experiences out of the equation or conclusion.  Take this statement, for instance, 
Doctors and scientists have long feared that general [anesthetic], mini-strokes or inflammation may damage the brain during surgery, but there has been evidence to show a long-term impact.  
What does that tell you when you read words like "Doctors and scientists have long feared"?  It tells me that doctors and scientists have known for a long time that surgeries destroy cognitive function.  Whereas the patient is only concerned about restoration, doctors and surgeons are only concerned about the money they earn from the surgeries.  These guys really are monsters, unthinking and unethical monsters.  I have made the point that I think that the modern-day medical industry is ground zero for the eugenics movement.  They will kill you, starting with your brain.  And the trouble with full benefited career positions is that newcomers to the American medical industry find the cornucopia of medical services like candy on display in a drugstore malt shop.  Medical services are the cherry on top of a messianic education that saved the individual from destitution, despair, and set them on the right path of production.  Now, with a career, the graduate is entitled to benefits, entry into a medicated eugenics movement whom we are told is for our benefit.  
Major surgery was also found to age the brain by an average of four months and three days. 
You see, it's statements like these that should cause most thinking, reasoning, rational human beings to pause, 
Assistant professor Robert Sanders, of the Department of Anesthesiology at Wisconsin, said: “The cognitive effects of surgery should be considered alongside the other potential health benefits of surgery. 
In effect, the statement instructs the patient to consider the cognitive effects of surgery "alongside the other potential health benefits of surgery."  Did you hear the wording there?  Note how the author coupled surgery with benefits and for the patient to weigh the cognitive effects of surgery.  Do you think that his doctor is going to be there trying to work his patient toward the surgery?  I know that that's what my doctors did with me on my knee surgery.  I went to three different doctors for an opinion.  Each one promoted surgery.  There was no dissenting voice, offering alternative remedies.  None.  It felt like a monopoly or a consortium or panel of doctors who'd all gone to the same conference.  Little did I know I was locked into a surgical cabal.  People laugh at me for being so cynical and sarcastic, but when I stop to think about how the medical industry has been little less than a tank battalion traipsing through the bodies of family and friends, how can one not be critical?  And still, I hear folks place an undying faith and an inordinate amount of trust in their doctors who know next to nothing about nutrition.  And what they do know, is often anemic.  

This next statement may be the most honest in the history of mainstream medical annals.  
Potential mechanisms of brain injury in the perioperative period include strokes, mini-strokes and inflammation.
What that statement does is present the concrete reality of brain damage from surgery--damage by way of a stroke, a mini-stroke, and inflammation.  Inflammation can be dealt with through vitamin C and fish oils.  One of my customers a few years ago was having surgery on her sinus cavity.  She was an attractive woman, articulate, buoyant in her late 50s but she was worried about going under the knife.  I told her not to because I think that the tendency of surgery is that it weakens the point of surgery as well as the distal points that intersect at the point of surgery.  Worried as she was, she still went through with the surgery.  I told that if she's going to go through with it that she should at least load up with vitamin C minutes before the surgery.  She acknowledged the value of that advice but failed to honor it.  

I am absolutely stunned by the honesty of some of the statements in this article.  Truly, it surprises me.  It seems rare and feels like a shift in values driven by economic and cultural shifts from the post-war entrenchment of that era's professional bureaucracies.  It feels like deregulation.  But deregulation does not occur satisfyingly toward more freedoms and improvements.  It may be a case of one step forward, two steps back.  Time will tell.  
Long-term cognitive health may also be influenced by postoperative pain and some medications. It is widely considered that anaesthesia may affect long-term cognition but this has not been strongly supported by the recent literature. 
The article leads with "Doctors and scientists have long feared that general [anesthetic] . . . may damage the brain during surgery [including] . . . evidence to show a long-term impact."  Then here it adds that "It is widely considered that anaesthesia may affect long-term cognition but this has not been strongly supported by the recent literature."  Well, okay, genius, what literature?  Where?  How does one measure "strongly supported"?  What are the criteria for "strongly supported"?  Oh, that is a topic for another article, is that it?  Bait people and let them die on the vine.  So, note what this and other authors of their kind do.  They make a claim and then temper it with "but this has not been strongly supported by the recent literature."  What about historical literature?  What does that say about the effects of surgery?  I mean if anyone is thinking AT ALL about this, one can only surmise that the medical industry is filled with degreed idiotic automatons.  You can probably get better healthcare, I mean real health care, from a tribal shaman in Uganda.  

Oh, I loved this next remark, "“Unfortunately we are unable to study the mechanisms more fully in this dataset and we are conducting new studies to understand this better.”  Just as the author is making the case for dementia-like symptoms resulting from "major" surgery [I will add most surgeries], Ms. Sarah Knapton backs off from her conclusions for fear that she is offending the powerful cabal or commission or panel or medical monopoly by making statements that might cause a tectonic shift in their practices and rationale.

What I did learn from this article, notwithstanding the back-and-forth assertion-denial dog and pony show, was the aging of the brain from surgery can be extensive and long-term.  
During that 19 year period, 1,250 were admitted to hospital for major surgery, and after accounting for age-related cognitive decline, the authors calculated that major surgery was associated with an extra decline of just over four months.
Being admitted for a medical condition, such as a heart attack, also brought a mental decline of 1.4 years, while a stroke aged the brain by 13 years. 
This is why a stroke is so devastating.  And the best prevention, supplement-wise is methylcobalamin, i.e., B12.  You would think that with the devastating impact of surgery and post-surgery risks that Ms. Knapton could offer some remedy.  Alas, that's not what the medical literature is all about.  At least Ms. Knapton is consistent with the see-saw effect of her message, 
Fiona Carragher, Chief Policy and Research Officer at Alzheimer’s Society, said: “The main message to take from this study is that major surgery isn’t as bad for your cognition in midlife as some people might fear. The effect is slight – only speeding up the normal cognitive decline that occurs in ageing by five months. 
Oh, I see.  Now major surgery "ISN'T AS BAD FOR YOUR COGNITION IN MIDLIFE AS SOME PEOPLE MIGHT FEAR."  Glad that was cleared up.  So it isn't AS BAD?  So does that mean that it still IS BAD but just not AS BAD?  How bad are we talking about?  Bad.  Bad.  It's bad.  Inflammation bad?  Mini-stroke bad?  Macro-stroke bad?  Yeah, it's bad; that's bad.  

Then as Ms. Knapton waffles (I mean she really does have to, doesn't she, I mean if she wants to keep writing in the medical field, right), she leans on that old standby of anonymous authority of "studies show."  "Also, the study is limited, it gives us little information on their reason for a hospital stay, how severe their stroke was and we don’t know if they went on to develop dementia so cannot provide any information on dementia cause or risk."  "It gives us little information on their reason for a hospital stay . . ."?  Is she serious or is this a case of playing naive?  Everyone I've known who've been instructed by their doctor or by an emergency doctor to STAY in a hospital is because the patient had great insurance, and the hospital treats them like lab rats AND an ATM machine.  Ka-ching I believe is the reason for a hospital stay.  Go ahead, Ms. Knapton, say it.  The eugenics movement is a profitable gig.  

I don't think that I've read an article where the waffling has had such an ambiguous conclusion.  It's like reading a letter penned by a character in an Edgar Allan Poe story.  Check this out.  "“We know from our own research that hospital admissions and the state of delirium that can result from extended stays can have a negative impact on cognition among people with dementia."  So in the previous statement, Ms. Knapton asserts "that major surgery isn’t as bad for your cognition in midlife as some people might fear," then underscores her earlier and initial claim that "We know from our own research that hospital admission and the state of delirium that can result from extended stays can have a negative impact on cognition among people with [meaning those who already suffer from] dementia."
Okay, enough of my cynicism. 

Isn't that just wonderful?  Imagine all of the folks who've been sold by their doctors that a particular surgery was needed either to save their life or to save an organ or to improve a condition.  that this and that surgery is not only good for you but necessary.  And doctors recommend unnecessary surgeries without ever providing you with healthier, more natural remedies. 

Post-operative cognitive decline in older patients, apparently, has been known well and long.  NCBI observes
Older patients, in particular, are vulnerable to memory disturbances and other types of cognitive impairment after surgical operations. In one study, roughly 12% of patients over age 60 had postoperative cognitive dysfunction (POCD) three months after surgery. This is an important issue in perioperative care as extensive surgery on older patients becomes more common. 
It looks like anesthesia is the main cause of cognitive decline.  I must be a case that the anesthesia makes it harder for people to recover from the general malaise of anesthesia.  
Cognitive impairment after anesthesia and surgery (postoperative cognitive dysfunction, [POCD]) is a recognized clinical phenomenon.



UPDATE: SOLUTIONS TO COGNITIVE IMPAIRMENT THAT RESULT FROM SURGERY.
We all know the value of B vitamins for improving nerves and muscle health.  How many of us have taken a B complex?  I know I have.  And as beneficial as the B complex is, it is not enough.  Here's why: the form of B vitamins that are in a B complex are usually water-soluble forms, like Thiamine, Niacin, Folic Acid, B5, B6, B9, and others.  What is more effective are fat-soluble B vitamins.  The fat-soluble version of Thiamine is called Allithiamine, and this, according to British doctor, Dr. Derrick Lonsdale, repairs the autonomic nervous system.  Martie Whittekin in her latest show and interview with Bill Sardi writes
(The oil-soluble forms of vitamin B1 we will discuss are benfotiamine and allithiamine the one that gets to the brain.) We will also explore good reasons (and some not so logical) for taking an anti-aging pill. The science is surprising. Read Mr. Sardi’s article on this topic. 
Sardi in his own article explains that 
. . . a single nutrient, thiamine (thii-ah-meen) vitamin B1, by virtue of its ability to facilitate the transport of oxygen on hemoglobin (the red oxygen-carrying pigment in red blood cells), as the antidote to eye, nerve, heart, brain and lung disorders. 
So, the better Thiamine form is the fat-soluble allithiamine.  Get it today if you want vitality.  Truly.  Citing a report by Derrick Lonsdale, Sardi says that most of us are vitamin B1 deficient.  A serious deficiency can cause beriberi.  Check out the symptoms of that.  Pretty serious.  Sardi emphasizes that we may be getting adequate INTAKE of B1 through our diet and from our multi-vitamins, but that eating of lots of carbohydrates like sugar, pasta, breads, rice, cereals, coffee, tea, sodas, alcohol, high-fructose corn syrup, and "bacon and peanut butter and prepared meats and just about everything else" means we're not ABSORBING enough B1: we may be consuming adequate amounts, but we're not absorbing it.  

THE RESULT?  And most of us are losing control of our autonomic nervous system; we develop dysautonomia through high-calorie malnutrition.  The autonomic nervous controls our breathing, heart rate, defecation, digestion, bowel movement, blood pressure, body temperature, sweating, tears, saliva, and more.  When we don't have vitamin B1, our autonomic nervous system gets out of whack.  We will experience heart flutters, digestion, mood, and blood pressure, nervous conditions, sleep--both the lack and oversleeping.  

Lonsdale explains that modern medicine has organized itself anatomically, according to individual organs, rendering medicine individualized and highly specific which is good.  We have cardiologists for the heart, neurologists for the central nervous system, ophthalmologists for the eyes, and so forth.  What this means is that no one is paying attention to the overall network effect of your nerves--the autonomic nervous system.  However, the autonomic nervous system encompasses every one of our organs.  A patient can go to 5 to 7 different doctors for different conditions but the origin of the problem, lack of vitamin B1, can go undiagnosed.  It's systemwide, and we can't get a handle on it.  We can treat the symptom but we can't treat the cause.  Sardi explains that there are 696 published papers where they've tried to use vitamin B, Thiamine, for 230 different diseases.  Of course, they've tried it because it is the cause of all of these!  In a society eating carbohydrates, drinking alcohol, even drinking coffee and tea, and these have blocked the absorption of Thiamine, B1.  Now, these perplexing diseases, which have affected all of us.  This was interesting: Thiamine was historically confined to prison camps where people didn't have the food, for alcoholics, and where starvation existed.  Now, it's widespread, and Lonsdale calls this widespread chronic-disease effect "high-calorie malnutrition."  Cardinal signs of B1 deficiency?  Swelling, nerve problems, circulatory problems.  Thiamine enables our cells to make energy in our mitochondria.  About 34% of pharmaceuticals impair the mitochondria.  Thiamine makes it possible to make energy.  Inadequate B1 impairs cell energy.  It critically impairs hemoglobin to carry red cell oxygen.  

Nausea is a lack of thiamine!  Memory loss, delirium, goosebumps, mental depression, insomnia, the list goes on and on--it is exhaustive.  Retina eye problems, Parkinson's disease.  Dr. Lonsdale says of the most severe forms of vitamin B1 deficiency are missed, so we're talking about something widespread.  Various points of stress in your life.  Factory workers in Japan took off the hull or bran of the rice, and they would go outdoors and in between two buildings they would shield themselves from sunlight until about noon when direct sunlight reached the earth's floor and struck them.  They all had different symptoms--hives, outbreak--all the result of a lack of vitamin B1.  The sun became a stressor.  You do not have the capacity to send the oxygen to produce cell energy and all of this produces sepsis because they can't stop the sepsis.  They're trying to treat it with vitamin B1 and vitamin C.  Why so many cases of sepsis now?  Because we don't have enough.  

In the 1930s, men taking B1 would have their dark hair return with Benfotiamine.  If you're going to drink coffee, then you take the Benfotiamine or Allithiamine or Sulbutiamine in the afternoon, away from your morning coffee.  You're going to keep your dark hair.  Allithiamine pierces the brain-blood barrier.  Benfotiamine does not, however, it is noted by Alzheimer's doctor by its ability to take away brain plaque and lack of memory in Alzheimer's patients.  Out of 150mgs, the body only absorbs 5mgs.  Coffee, tea, and water are diuretics interfere with its absorption, so take magnesium and zinc to increase its absorption.  Allithiamine gets to the blood-brain barrier.  If you have a serious disorder, you may want to take that for a while.  You are going to overcome some of these diseases.  You need some zinc.  Our heart beats without our conscious control.  In this study co-authored by Lonsdale, it looks as though Thiamine also solves autism.  

B1 is the first vitamin ever discovered in 1889.  Here is a little more background on Thiamine, its best food sources, and its uses.  

Monday, July 15, 2019

"BY TAKING GOOD ANTIOXIDANTS, YOU CAN INACTIVATE THE NEGATIVE EFFECTS OF RIBOFLAVIN WHILE GETTING ITS BENEFITS"


from the DailyMail.co.uk
Doctors have restored sight to the blind by sending video images directly to the brain.
In a world-first that offers hope to millions of patients, five men and one woman have regained vision after years of ‘living in the dark’.
They had electrode chips planted in the visual cortex at the back of their skulls that picked up images from a tiny video camera mounted in a pair of glasses. Their eyes were bypassed completely.
One of the participants, Benjamin James Spencer, who went blind aged nine, described his joy at seeing his wife and three daughters for the first time. ‘It is awe inspiring to see so much beauty,’ the 35-year-old told the Daily Mail last night. ‘I could see the roundness of my wife’s face, the shape of her body.
‘I could see my kids running up to give me a hug. It is not perfect vision – it is like grainy 1980s surveillance video footage. It may not be full vision yet, but it’s something.’ 
Mr. Spencer described how, when he was nine years old, his world went black.
‘It was September 18, 1992, a week after my birthday,’ he said. ‘I was at school leaving a class and in the time it took me to walk 50ft everything disappeared.
‘At first it started to go foggy and then a few paces later it was just dark.
‘I panicked and started screaming and kind of went into shock. Everything after that is pretty vague.’
In the coming days, specialists at a hospital near his home in Texas broke the news that he would never see again.
‘I was told this was going to be my future. I was classed as lacking 100 percent light perception. I was blind,’ he said.
Mr. Spencer had pediatric glaucoma, a rare condition caused by a defect in the eye’s drainage system.
·         


Ben Spencer, 35, with his wife and daughters (left to right: Melissa, 13, Jeanette, 42, Jane, 10, and Abigail, 15)
It had been incurable but scientists have now managed to bypass the broken link by sending images directly to the visual cortex, the part of the brain responsible for sight.
Mr. Spencer lives in the city of Pearland, near Houston, with his wife Jeanette, 42, and daughters Abigail, 15, Melissa, 13, and Jane, ten. In April 2018, he became one of just six people to have a 60-electrode panel implanted in the back of his brain.
Surgeons at Baylor Medical College in Houston spent two hours cutting a window in his skull, placing the electrode array on the surface of the brain, and stitching it up again. They then spent six months ‘mapping’ his visual field.
This involved sending computer signals to the stimulation panel in his head to synchronize his brain to the real world – in effect teaching his visual cortex to process images again.
Eventually, in October, the device was wirelessly connected to a tiny video camera, mounted in a pair of glasses, and switched on. He saw his wife and three children for the very first time.
‘It was an incredible moment,’ he told the Daily Mail. ‘It was very humbling.’
Describing catching a glimpse of the sun through the window, he said: ‘Such a tiny thing is normal for people who have vision. But I had not seen the sun since I was nine years old. I had felt its heat, but actually seeing it was incredible. After 25 and a half years of living in the dark, it is awe-inspiring to see so much beauty.’
In January, after months of hospital testing, he was allowed to take the device home. The terms of the clinical trial mean he can only switch it on for three hours a day, but he makes the most of it. ‘I usually use it for 45 minutes at a time and space it out,’ he said. ‘If I want to go to the store or if one of my kids has a performance.
‘It is not perfect vision – it is like grainy 1980s surveillance video footage,’ he said.
‘I can see silhouettes, I can see light and shade, I can guess at colors. It may not be full vision yet, but it’s something.
‘I can go to the store, I can walk without my cane, I can sort my dark laundry from the whites, I can see a crack in the sidewalk coming up. I could see a sign sticking out – but I couldn’t read what it said.’
Even when completely blind, Mr. Spencer learned to thrive independently.
He finished school, went to college and earned a masters in business, focusing on international trade. He worked for a few years in import-export and then set up his own tax business.
‘I was determined to be an independent person,’ he said. ‘There is always a way around whatever the world throws at you.
‘Luckily I had people around me who said you can allow this to define you, or you can define life. But that being said, everything was a stepping stone. I learned that life was about adaptation.’
British experts described the breakthrough in the United States as a ‘paradigm shift’ in the treatment of the blind.
Patients who have benefited from the Orion wireless technology include those who have lost their sight due to glaucoma, trauma, infections, autoimmune diseases, and nerve problems.
But the surgeons – from Baylor Medical College in Texas and the University of California Los Angeles – believe they can eventually help anyone who has lost their sight. They are unsure, however, whether it could help people born blind – because the visual cortex would never have learned to process images.
They plan to implant 30 more devices over the next few months and if the results continue to be positive expect the technology to become widely available within three years.
Alex Shortt, a University College London lecturer and surgeon at Optegra Eye Hospital in the capital said: ‘This, to my mind, is a massive breakthrough, an amazing advance and it is very exciting.
‘Previously all attempts to create a “bionic eye” focused on implanting into the eye itself. It required you to have a working eye, a working optic nerve.
‘By bypassing the eye completely you open the potential up to many, many more people.
‘This is a complete paradigm shift for treating people with complete blindness. It is a real message of hope.’
Sibling pals: Mr. Spencer, as a young boy aged 7 with his sister Tiffany
He said the quality of the images would only improve.
Second Sight, the small American firm which makes the device, already has links in the UK thanks to another visual gadget trialed by the NHS. It plans to try to make Orion available here as soon as it is fully approved in the US.
Two million Britons have sight loss – 360,000 of whom are registered as blind. These figures are set to double by 2050.
Another patient in the trial was able to tell apart the different balls on a pool table, picking out the cue ball from the striped balls and even picking out the blue ball. Others can walk around a block unaided, avoiding cars and pedestrians, and tell the curb from the road.
Scientists hope to radically improve the quality of the device.
The current prototype has 60 electrodes. The version they hope to use in their next trial will have 150 – and in time this will go up.
Daniel Yoshor, the neurosurgeon at Baylor who implanted the device in Mr. Spencer’s brain, said: ‘When you think of vision, you think of the eyes, but most of the work is being done in the brain. The impulses of light that are projected onto the retina are converted into neural signals that are transmitted along the optic nerve to parts of the brain.’
The Orion device works by replicating that process with a video camera. The electrodes stimulate spots in the visual field – the ‘mind’s eye’ – which when working together create a black and white image that replicates the real world. Professor Yoshor said: ‘If you imagine every spot in the visual field, the visual world, there’s a corresponding part of the brain that represents that area, that spatial location.
‘If we stimulate someone’s brain in a specific spot we will produce a perception of a spot of light corresponding to that map in the visual world.
‘The idea is if we cleverly stimulate the individual spots in the brain with electrodes we can actually reproduce visual form, like pixels on an LCD screen.’
He added: ‘I tell these patients they’re like astronauts flying to the Moon, they’re taking bold steps to see not only if the device can help them as individuals, but if it can help the community of blind patients across the world.’
The results from the first six patients, presented at the World Society for Stereotactic and Functional Neurosurgery conference in New York a fortnight ago, revealed each patient had regained at least some degree of vision.
Second Sight is in negotiations with the FDA, the US health regulator, to launch another study in the coming months involving 30 patients.
Will McGuire, head of the firm, said: ‘We expect at least two to three years until it is going to be available commercially. That will be down to negotiations with the FDA. Then we will start discussions with regulatory bodies outside the US.’
The Orion system is built on the success of an earlier device called the Argus II, which uses a similar camera to send images to an implant at the back of the eye, restoring sight to people who have started to lose their vision to common conditions such as age-related macular degeneration – or AMD.
It hit the headlines when it was unveiled at Manchester Royal Eye Hospital five years ago.
But it relied on a patient having at least some working retinal cells, stimulating them with the video images and sending the signal through the optic nerve to the brain.
The new system takes the concept a step further – bypassing the eye completely and sending the images directly to the brain.
This means anyone could benefit, even if their eyes are irreversibly damaged or missing altogether – such as those who have lost an eye in an accident or on the battlefield, or those who have become blinded by cancer, meningitis or sepsis.
Helen Lee, of the Royal National Institute of Blind People, said: ‘We welcome this innovative technology which appears to have the potential to improve visual experience for people who are blind.
‘It could be life-changing for many people, but it is very early days.
‘Robust trials are needed to assess both the benefits and the adverse effects.’ And Professor Glen Jeffery, a visual scientist at University College London, said he doubted the new device would ever be able to restore more than very crude vision.
‘You may be able to see large objects, or large letters, and move around the world. Technology has moved on massively in this area. But people are not going to be able to read a newspaper with this.’
He said the retina was an extremely sophisticated part of the body – and simply bypassing it would not produce the kind of vision people expect.
‘It is also going to be extremely expensive to do this on many people,’ Professor Jeffery added.
End of article.  Excellent article for reactivating eyesight in adult men.  But if you want to keep your vision for a very long time, then you'll want to see what Bill Sardi recommends to fight off macular degeneration.  
The currently recommended dietary supplement (AREDS formula) formulated by the National Eye Institute for macular degeneration doesn’t appear to have any influence in preventing or slowing this disease as measured by the dark adaptation test.  [Retina April 27, 2017]
The only hope for therapy or prevention comes from a pilot study that showed a nutraceutical (Longevinex) reversed the progression of retinal aging as measured by the dark adaptation test.  [British Journal Medicine &Medical Research June, 2017; 8 NEWSNOW KLAS-TV/CBS Affiliate, June 15, 2017J.





Dr. Nan Fuchs, Ph.D. recommends water, sunglasses [amber shade of lens that blocks the UV and the blue light], and Hyaluronic Acid.  
A Remedy to Consider Our eyes shrink as we age from a loss of HA — a nutrient that keeps water in the vitreous humor. Optometrists and ophthalmologists say there’s no treatment for floaters and flashes and suggest we just live with them. They may be right. But I know of some people who have found that taking 150-300 mg of oral hyaluronic acid and drinking plenty of water reduced or eliminated their floaters. I’m not one of them. My floater and flashes continue after taking HA for five months.
Still, taking HA makes sense for your eyes and a number of other conditions such as arthritis. You can buy HA from Purity Products, Inc (800-769-7873). The supplement, Ultimate H.A. Remedy, contains a month’s supply of hyaluronic acid (at 150 mg a day) for $39.95. How long should you take it? No one really knows, but I like to give any supplement a three-month trial. If, after this time, there’s no change in your floaters, you’ve at least given your body a few month’s worth of an important lubricant.
Along with the hyaluronic acid, get plenty of antioxidants like bilberry, quercetin, vitamin C, grape seed, and glutathione. Your eyes contain the B vitamin riboflavin that’s needed to help you see light. Along with making your eyes more sensitive to light, riboflavin produces free radicals. By taking good antioxidants, like the Sharper Vision formula (800-728-2288) I use, you can inactivate the negative effects of riboflavin while getting its benefits. There are some people who believe that high amounts of riboflavin without enough antioxidants could contribute to floaters, although I haven’t been able to locate any studies that indicate this is so. Still, I believe in erring on the side of caution — so always take extra antioxidants in your diet and supplementation program for healthy eyes.
PROTECT YOUR EYESDrink plenty of water. Since floaters and flashes occur with changes in the vitreous, and vitreous is 99 percent water, drink plenty of water. Dehydration could be a factor in the vitreous separating from the retina. My own floater and flashes occurred after six weeks of persistent diarrhea from parasites. Although I was aware of needing plenty of fluids, it was difficult to be completely hydrated with daily watery stools, and I may well have been dehydrated. To prevent dehydration, drink half a glass of water an hour whenever possible.

Saturday, June 15, 2019

MANIPULATING RIPPLES TO ENHANCE MEMORY

Hippocampus Neuron, computer illustration Credit: Kateryna Kon Getty Images

Specific patterns of brain activity are thought to underlie specific processes or computations important for various mental faculties, such as memory. One such “brain signal” that has received a lot of attention recently is known as a “sharp wave ripple”—a short, wave-shaped burst of high-frequency oscillations.
Researchers originally identified ripples in the hippocampus, a region crucially involved in memory and navigation, as central to diverting recollections to long-term memory during sleep. Then a 2012 study by neuroscientists at the University of California, San Francisco, led by Loren Frank and Shantanu Jadhav, the latter now at Brandeis University, showed that the ripples also play a role in memory while awake. The researchers used electrical pulses to disrupt ripples in rodents’ brains and showed that, by doing so,  performance in a memory task was reduced. However, nobody had manipulated ripples to enhance memory—until now, that is.
Researchers at NYU School of Medicine led by neuroscientist György Buzsáki have now done exactly that. In a June 14 study in Science, the team showed that prolonging sharp wave ripples in the hippocampus of rats significantly improved their performance in a maze task that taxes working memory—the brain’s “scratch pad” for combining and manipulating information on the fly. “This is a very novel and impactful study,” says Jadhav, who was not involved in the research. “It’s very hard to do ‘gain-of-function’ studies with physiological processes in such a precise way.” As well as revealing new details about how ripples contribute to specific memory processes, the work could ultimately have implications for efforts to develop interventions for disorders of memory and learning.
The researchers first examined the properties of ripples recorded in rats performing tasks from a database acquired over years of experiments. They found more long-duration ripples occurred when rats had to make their way through mazes than when they were simply exploring or running along tracks. Negotiating mazes required rats to exercise their memories.
In one task, the M-maze, rats were trained to first navigate through the right-hand arm of a maze shaped as an “M” to receive a sugary reward, then through the left-hand arm on the next trial. The researchers saw significantly longer ripples in trials the rats performed correctly, compared to those they got wrong. “You can record a very simple electrical pattern in the brain and tell whether the animal's performance will be good or not, or whether the animal is learning or not,” Buzsáki says. These findings suggest that the hippocampus generates longer ripples during memory-intensive activities and that these longer-duration signals improve performance.
To verify that longer ripples contribute to better performance, the team artificially prolonged ripples in rats performing the M-maze task. The researchers used optogenetics, involving the use of light piped through a fiber-optic cable to activate genetically engineered light-sensitive neurons in the rats’ hippocampi. They recorded collective neural activity in the hippocampus during the task, to enable them to detect spontaneously occurring ripples. Upon detection of a ripple, light pulses were triggered to activate engineered neurons. This “closed-loop” stimulation roughly doubled the duration of ripples and significantly improved the rats’ performance, compared to control conditions with either no light stimulation or stimulation applied after short, random delays.
The rats also learned faster, reaching 80 percent correct performance in remembering which route would lead to a reward earlier than rats in the control conditions. The researchers also switched off any beneficial effects by aborting ripples using high-intensity light pulses, confirming that performance was impaired. “It's really nice to see another group do something slightly different and get the same result,” Frank says. “It makes you feel confident we're all on to something.”
To investigate how longer ripples might be enhancing performance, the team inspected the properties of the neurons involved. A ripple is not simply the repeated activity of the same neurons oscillating over time; instead, its activity spreads to more neurons as the signal continues.
The team observed that particular neurons tend to “fire” either in the early or in the later portion of the signal, and they found intriguing differences between these two groups. “Early” neurons were “chatterboxes” with high baseline activity, whereas “late” neurons were more sluggish, with lower average activity. “Neurons that fire fast are like talkative people, they are active in many situations,” Buzsáki explains.  “The majority typically don't fire, but once they do, they say something important.”
The hippocampus contains neurons specialized for navigation, called “place” cells, which fire when an animal is in a specific location. The researchers found that neurons firing in the late part of long ripples (either spontaneously occurring, or artificially prolonged), were more highly tuned to location, and the spots tended to be on the arms of the maze. Previous research suggests one function of ripples may be to “replay” memories. The new findings support that idea and suggest that prolonging ripples recruits extra neurons to generate the signal, whose activity is relevant to the task at hand. “When they extend the length of ripples, they’re recruiting cells that are reactivating paths the animals take,” Jadhav explains. “This might be a mechanism for doing a cognitive search of all the available paths, that other brain areas can read out and act on.”
The researchers hope this work eventually may help develop ways to treat the type of memory problems that occur in age-related cognitive decline or Alzheimer’s disease. Learning difficulties might also be addressed. The techniques in the experiments would be tricky to apply to humans because they are invasive and involve genetic manipulation, but Buzsáki says they are working on noninvasive methods. A recent study, published in April and led by neuroscientist Robert Reinhart of Boston University used weak electrical currents applied to the scalps of elderly participants to obtain an increase in working memory performance, accompanied by greater synchrony between oscillations of certain (theta) frequencies in different cortical regions. “There are intriguing points of connection between the elegant work by [Buzsáki’s team] and research conducted in my laboratory,” Reinhart says. “Research in systems and cognitive neuroscience is laying critical basic science groundwork, which may open up an entirely new avenue of circuit-based therapeutics for the prevention and treatment of brain disorders.”
The problem with existing non-invasive methods, such as transcranial magnetic stimulation (TMS), or the transcranial electrical stimulation (TES) technique, used in Reinhart’s study, is their inability to  penetrate into the brain, so manipulating signals in the deeply seated hippocampus is difficult. Recording from deep in the brain non-invasively is even more tricky. One possible solution would be to infer when ripples occur in the hippocampus from activity recorded from the brain’s surface. “There might be a very specific pattern of, say, prefrontal activity that precedes these events” and produces ripples in the hippocampus. Frank says. "But we don’t understand what that looks like yet.” 
Also, modifying cortical activity using these techniques may, as a consequence, affect activity in the hippocampus. “We know that these sharp wave ripples can be biased by [specific] neocortical patterns,” Buzsáki says. “In fact, many companies are trying to affect memory, by changing neocortical patterns.” Finally, invasive methods, similar to implants used to detect and interfere with seizures in epilepsy, could be employed, either for detecting, or manipulating ripples, or both. Invasive and non-invasive methods could even be combined. “As long as you can measure these events and come up with some way to manipulate them, you have the possibility of making the system work better,” Frank says. “There's a world of possibilities there.”
Note: György Buzsáki's affiliation was corrected from "New York University" to "NYU School of Medicine." 
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