The New Symptom Of Alzheimer’s Disease.


 

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Too much tossing and turning could be a sign of trouble to come. Restless nights may signal the onset of Alzheimer’s disease years before memory loss or other cognitive problems occur, shows intriguing new research published in Neurology.

For two weeks, a study team tracked the sleeping habits of 145 healthy adults. The researchers also tested the participant’s spinal fluid for markers of preclinical Alzheimer’s. Those who scored lowest in terms of overall sleep quality were five times more likely to test positive for preclinical Alzheimer’s. Signs of poor sleep quality include taking more time to fall asleep, sleeping less during the night, and taking naps more frequently during the day, according to the study.

What might sleep have to do with Alzheimer’s? Small amyloid plaques are present in the brains of sufferers, and may appear up to 20 years before cognitive decline sets in, says study co-author Yo-El Ju, MD, a neurologist at Washington University in St. Louis. These plaques appear to interfere with the neuronal functions necessary for healthy sleep. That means trouble sleeping—even in your 40s or 50s—could be cause for concern, the study suggests.

And there’s more bad news: Not only do these plaques disrupt sleep, but sleeping poorly also appears to increase their presence, meaning it may contribute to the development of Alzheimer’s, Dr. Ju explains. Fortunately, she says understanding the relationship between sleep and Alzheimer’s could help doctors develop treatments to slow or stop the development of the illness.

There’s no cure for Alzheimer’s, but getting a good night’s rest could slow the buildup of brain plaques that leads to cognitive decline, the research suggests. If you’re struggling with sleep woes, Ju recommends avoiding caffeine and alcohol, establishing a consistent sleep schedule, and following other well-established sleep-improvement tips. If those tactics don’t work after several weeks, then she suggests talking to your doctor about the problem. Of course, it may very well not signal Alzheimer’s—but poor sleep is also linked to other health conditions, like heart disease and diabetes.

Source: socialreader.com

 

 

Long-term evolution is ‘surprisingly predictable,’ experiment shows.


 

A protein-folding simulation shows that the debated theory of long-term evolution is not only possible, but that the outcomes are predictable. The Stanford experiment provides a framework for testing evolutionary outcomes in living organisms.

Two birds are vying for food. One bird’s beak is shaped, by virtue of a random mutation, such that it’s slightly more adept at cracking seeds. This sets the bird on the road toward acquiring more food, a better chance of scoring a mate and, most important, passing on its genetic endowment. This individual’s success is an example of short-term evolution, the widely accepted Darwinian process of natural selection by which individual organisms that have better adapted to their surroundings prevail. In recent years, however, some scientists have argued that natural selection occurs not just at the individual organism level, but also between lineages over the course of many generations. In a new study, Stanford biologists have demonstrated that not only is this long-term evolution possible, but that long-term evolutionary outcomes can be surprisingly predictable. The group set up a computer simulation in which 128 lineages of proteins continuously folded into new shapes, competing to bind with other molecules, called ligands, in each new configuration. The better each protein could attach itself to the ligands, the more ligands it would scoop up, and the higher its fitness – that is, its average number of “offspring” – would be. The simulation was run for 10,000 generations. Although the chaos of 128 lineages – a total of more than 16,000 individual proteins – mutating over thousands of generations might seem unpredictable, and that it would be nearly impossible for the same thing to happen twice, it’s actually the opposite. “Even though things look complicated, the possible evolutionary trajectories are quite constrained,” said lead author Michael Palmer, a computational biologist at Stanford. “There are only a few viable mutations at any point, which makes the dynamics predictable and repeatable, even over the long term.” Ads by Google Submit Your Resume – 2-10 years Exp. Salary 3-15 Lakhs. To Apply, Register on Shine.com Now – Shine.com/Pharma_Jobs The study, co-authored by Marcus Feldman, a biology professor at Stanford, and Stanford research biologist Arnav Moudgil, was recently published in the Journal of the Royal Society Interface. In some experiments, the lineages that consistently came out on top in the long term were not initially the best adapted at binding to ligands. “The immediate fitness is not the only important thing,” Palmer said. “Yes, a lineage does have to survive in the short term. But just as important is how it is able to adapt to new and potentially variable environments over the longer term.” A good example of this scenario is Darwin’s famous finches. It’s thought that individuals – perhaps just a single pair of birds – from a South American species ended up on the Galápagos Islands about 1 million years ago. Today their descendants have diversified into about 15 modern species. Some eat seeds, some eat insects, or flowers. Some eat ticks, or even drink the blood of other birds. “If there was some catastrophe that removed one of those food sources, it might wipe out one or more of the 15 species, but the rest of the lineage – the descendants of that initial pair of birds – would persist,” Palmer said. “Now say there was a competing lineage that was great at cracking seeds, but unable to evolve to other diets due to some prior genetic constraint. The same catastrophe could wipe it out.” The finding, and others like it, could represent a significant shift in viewpoint for biologists. For one thing, it means that in certain situations, scientists should look beyond the details at the level of the individual organism, as the evolutionary dynamics can be accurately understood as lineage selection. It also has implications on a species’ genomic architecture, or how a genome is organized on the lineage level. While a lineage’s genome might primarily select for a particular set of traits in order for individuals to survive in the short term, in order to out-compete other lineages, it must also be able to adapt to new conditions over the long term. “An individual can have a lucky mutation that produces an immediate adaptation,” said Palmer. “Or a lineage can have a lucky mutation that happens to position it to adapt to the range of environments it will experience over the next thousand generations. A single mutation can have a distinct short-term and long-term fitness.” The authors believe that the work can be replicated in microorganisms, and are now hoping that microbiologists will apply the new metrics of selection in vitro. “There is already some evidence in vitro that there is a lot of constraint on evolutionary trajectories,” Palmer said, “and we think we’ve come up with a good framework to quantify evolutionary predictability and long-term fitness

Source: Journal of the Royal Society Interface

 

‘Star Trek’ Prototype Tractor Beam Developed By Scientists.


 

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It may still be a few years away from practical use, but scientists have created a real tractor beam, like the ones featured in the “Star TrekTV series and movies.

Simply put, this technology utilizes a beam of light to attract objects, according to theUniversity of St. Andrews in Scotland. In “Star Trek,” tractor beams were often used to pull spaceships and other objects closer to the focal point of the light source attached to another ship.

Researchers at St. Andrews and the Institute of Scientific Instruments, or ISI, in the Czech Republic have figured out a way of generating an optical field that can reverse the radiation pressure of light.

German astronomer Johannes Kepler noticed in 1619 that comet tails point away from the sun, a radiation force that the St. Andrews and ISI team hoped to reverse.

According to the BBC, Pavel Zemanek of ISI said, “The whole team have spent a number of years investigating various configurations of particles delivery by light. I am proud our results were recognised in this very competitive environment and I am looking forward to new experiments and applications. It is a very exciting time.”

So far, based on their research findings published in Nature Photonics, the team is able to move tiny particles, on a microscopic level.

Team leader Tomas Cizmar, of the St. Andrews School of Medicine, said the new technology has great potential.

“The practical applications could be very great, very exciting,” Cizmar told the BBC. “The tractor beam is very selective in the properties of the particles it acts on, so you could pick up specific particles in a mixture. Eventually, this could be used to separate white blood cells, for example.”

While the researchers hope this tractor beam technology will be useful in the medical field, they don’t anticipate it can ever be used to capture and haul large objects like spaceships.

“Unfortunately, there is a transfer of energy. On a microscopic scale, that is OK, but on a macro scale, it would cause huge problems,” said Cizmar.

“It would result in a massive amount of heating of an object, like a space shuttle. So trapping a spaceship is out of the question.”

Tractor beam concepts have been experimented with before.

In 2011, a NASA-funded study examined how special laser beams might be used to capture and gather sample materials on unmanned, robotic space missions,Space.com reported.

“Though a mainstay in science fiction, and ‘Star Trek’ in particular, laser-based trapping isn’t fanciful or beyond current technological know-how,” Paul Stysley of NASA’s Goddard Space Flight Center said at the time.

And in 2012, New York University physicists David Ruffner and David Grier developed a way to use special lasers, called Bessel beams, to direct light in concentric circles at an object — albeit a 1.5-micrometer silica sphere — and the beams could then reconstruct themselves on opposite sides of the sphere, making it possible to pull the object back to the source of the beams.

The only problem with this theory is that, like the current tests by the scientists at St. Andrews and ISI, applying these techniques to move very large objects isn’t practical yet — the huge energy requirements to make it work would destroy the objects trying to be pulled.

Source: http://www.huffingtonpost.com

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Meteors Don’t Strike Twice.


Without precedent or warning, a loud boom sounding like a major piece of artillery frightens your normally quiet neighborhood. Houses shake and dishes rattle. The jolt is singular, percussive — and ominous. Later the TV news reports that the boom was heard over many miles, but nothing exploded. No supersonic aircraft flew by. Someone saw yellow light in the sky.

Residents of New York’s Rockland and Westchester Counties, not far from New York City, experienced this in March 2009. It could have been a rare, beach ball sized meteor that disintegrated before it hit the ground. Meteors are certainly supersonic and have been known to make loud sonic booms. A bounty hunter offered $10,000 for a piece of the meteorite.

But the meteor theory blew up a couple days later. Another loud boom in the same area jolted people awake at 5:15 am. Nanuet resident Keith Wallenstein said of the second boom. “The house was shaking. It sounded like someone had flown an F-16 over the house. If it was thunder, it had to be right on the house. [But] I know a bunch of people who heard it within 3 to 4 or 5 miles away.”

By now you may be thinking the military was up to something after all. They’d be mum about it, wouldn’t they?

In James Fenimore Cooper’s day there were no supersonic aircraft. As he recounted in 1850:

The ‘Lake Gun’ is a mystery. It is a sound resembling the explosion of a heavy piece of artillery, that can be accounted for by none of the known laws of nature. The report is deep, hollow, distant, and imposing. The lake seems to be speaking to the surrounding hills, which send back the echoes of its voice in accurate reply. No satisfactory theory has ever been broached to explain these noises. Conjectures have been hazarded about chasms, and the escape of compressed air by the sudden admission of water; but all this is talking at random, and has probably no foundation in truth. The most that can be said is, that such sounds are heard, though at long intervals, and that no one as yet has succeeded in ascertaining their cause.

Cooper was talking about Lake Seneca, one of the Finger Lakes in upper New York State. The Lake Gun was the name given to the booms by local settlers. The Native Americans said it was their god talking.

Moodus, Connecticut is another hot spot for loud booms, and other noises too. The Native Americans there called the area Machemodus, or Place-of-Noises, and warned the early settlers about them. The Moodus noises ceased in the 1980’s but sprang back to life in 2011. In 1979 Boston College’s Weston Observatory set up seismometers and measured Moodus quakes producing pops or bangs more than a hundred times too small for people to feel, some as low as minus 2 on the Richter scale. The geologists found that the source of the quakes is in hard bedrock only 1500 meters deep under Moodus, very shallow for an earthquake. They offered no explanation for the sound.

Quakes hundreds or thousands times more powerful occur elsewhere yet are nearly silent. More powerful quakes, ones that start to do damage do make noise, but more like rolling rumbles, not singular explosions. Why should some quakes produce percussive booms so efficiently?

The booms are not caused by an explosion nor any material object moving supersonically. Instead they are launched by the world’s largest loudspeaker: the ground or surface all around you, especially if it is hard bedrock or water (water is actually very stiff-try compressing it!).

This is apparently controversial. A website devoted to the Guns of Barisol, India, on the northern shore of the Bay of Bengal, another place of bewildering sonic booms, tries to inoculate readers against the microquake explanation of the booms: “You may read . . . that the Guns of Barisal are supposed to be caused by earth movements too feeble to be felt. Earthquakes can make noises, but not when no movements are felt….” Actually this statement is quite false: small quakes can produce loud booms.

Oddly, the surface does not need to move very far nor very fast to launch exceedingly loud sound resembling cannon fire or a sonic boom. What it does need is a lot of acceleration. But how can something have huge acceleration, yet not wind up moving very far or very fast?

The answer is the acceleration must be very brief. Suppose the ground accelerates at 1000 G’s straight up before recoiling and reversing direction, all in 1000th of a second. (The Tesla Roadster, capable of 0 to 60 in 3.2 seconds, accelerates 1000 times less at under 1 G) If the ground or water surface does that, its speed is never more than a modest 1 meter per second, and it will move less than a millimeter! But one heck of a loud boom will be launched if large surface areas do that.

Acceleration is the agent of sound production. An accelerating surface “surprises” the air next to it and launches a pressure wave moving at the speed of sound, even though the surface and the air itself never comes close to moving that fast. When your fingernail touches a desktop, you hear an audible clack. The surface of the desk clearly never moves very far, and the desktop certainly doesn’t move any faster than your fingernail was moving, but the sudden contact of desk with fingernail causes a significant (many G’s ) but short lived acceleration of the desktop, which launches the sound.

A sudden breaking of a large piece of rock under great tension sends out a sharp compression wave moving fast in the rock — like a sound wave, only in rock. When the wave reaches the surface, the surface is very suddenly pushed up over a large area- a huge but short lived acceleration — and a boom in born.

Sharp waves traveling in rock tend to quickly round off, so the pulse and the acceleration will be reduced unless the quake is very close to the surface, as it is in Moodus, and presumably under Rockland and Westchester Counties, Seneca Lake, etc. A Richter 1 quake is plenty to launch an ear splitting boom if it occurs close to the surface, yet at Richter 1, the geologists won’t dignify the quake with a mention.

Source: http://www.huffingtonpost.com

Six Steps to Healthier Kidneys.


Most Americans know that heart disease and cancer can be silent killers and understand that monitoring blood pressure and cholesterol are critical to protecting their health. Too few adults—and not enough doctors—realize, however, that chronic kidney disease (CKD) is another common, life-threatening illness that often goes undetected until very advanced when it could be diagnosed early through simple tests.

Studies report that 26 million Americans suffer from CKD and millions more are at risk. Worse, today’s epidemics of diabetes and obesity could contribute to even higher rates of CKD in the future. Undiagnosed and untreated, CKD can lead to serious health problems including kidney failure. Caught early, it can often be managed, and kidney damage can be slowed or stopped. That’s why early testing for people at risk is so important.

In preparation for National Kidney Month and World Kidney Day, the NKF offers this 6-step primer for protecting health.

Step 1: Know These Facts

6 Things Healthy Kidneys Do:

  • Regulate the body’s fluid levels
  • Filter wastes and toxins from the blood
  • Release a hormone that regulates blood pressure
  • Activate Vitamin D to maintain healthy bones
  • Release the hormone that directs production of red blood cells
  • Keep blood minerals in balance (sodium, phosphorus, potassium)

8 Problems CKD Can Cause:

  • Cardiovascular diseas
  • Heart attack and stroke
  • High blood pressure
  • Death
  • Weak bones
  • Nerve damage (neuropathy)
  • Kidney failure (end-stage renal disease, or ESRD)
  • Anemia or low red blood cell count

 

Step 2: Assess Your Risk

4 Main Risk Factors:

  • Diabetes (self or family)
  • High blood pressure (self or family)
  • Cardiovascular disease (self or family)
  • Family history of kidney disease or diabetes or high blood pressure

10 Additional Risk Factors:

  • African-American heritage
  • Hispanic, Asian, Pacific Islander heritage
  • Age 60 or older
  • Obesity
  • Low birth weight
  • Native American heritage
  • Lupus, other autoimmune disorders
  • Chronic urinary tract infections
  • Kidney stones
  • Prolonged use of NSAIDs, a type of painkillers, such as ibuprofen and naproxen

 

Step 3: Recognize Symptoms

Most people with early CKD have no symptoms, which is why early testing is critical. By the time symptoms appear, CKD may be advanced, and symptoms can be misleading. Pay attention to these:

8 Possible Trouble Signs:

  • Fatigue, weakness
  • Difficult, painful urination
  • Foamy urine
  • Pink, dark urine (blood in urine)
  • Puffy eyes
  • Swollen face, hands, abdomen, ankles, feet
  • Increased thirst
  • Increased need to urinate (especially at night)

 

Step 4: Get Tested

If you or a loved one belong to a high-risk group, ask your primary-care physician about these tests—and be especially insistent about the last one. Your doctor may want to perform other tests as well.

What: Blood Pressure
Why: High blood pressure can damage small blood vessels (glomeruli) in the kidneys. It is the second-leading cause of kidney failure after diabetes.
Good Score: Below 140/90 is good for most people. Below 130/80 is better if you have chronic kidney disease. Below 120/80 is best.What: Protein in Urine
Why: Traces of a type of protein, albumin in urine (albuminuria) is an early sign of CKD. Persistent amounts of albumin and other proteins in the urine (proteinuria) indicate kidney damage.
Good Score: Less than 30 mg of albumin per gram of urinary creatinine (a normal waste product)

What: Creatinine in Blood (Serum Creatinine)
Why: Healthy kidneys filter creatinine (a waste product from muscle activity) out of the blood. When kidney function is reduced, creatinine levels rise.
Good Score: 0.6 to 1.2 mg per deciliter of blood, depending on other variables

What: Glomerular Filtration Rate (GFR)
Why: This is the most sensitive and accurate gauge of kidney function.Doctors measure blood creatinine levels and perform a calculation based on age, race, and gender.
Good Score: Over 90 is good. 60-89 should be monitored. Less than 60 for 3 months indicates CKD.

 

Step 5: Stay Healthy

6 Things People with CKD Should Do:

  • Lower high blood pressure
  • Moderate protein consumption
  • Avoid NSAIDs, a type of painkiller
  • Reduce salt intake
  • Get an annual flu shot
  • Keep blood-sugar levels under control if diabetic

9 Things Everyone Should Do:

  • Exercise regularly
  • Control weight
  • Follow a balanced diet
  • Quit smoking
  • Drink only in moderation
  • Stay hydrated
  • Monitor cholesterol levels
  • Get an annual physical
  • Know your family medical history
  • Prolonged use of NSAIDs, a type of painkillers, such as ibuprofen and naproxen

 

Step 6: Learn More

  • The National Kidney Foundation will offer free kidney screenings through its Kidney Early Evaluation Program (KEEP) for people at risk for CKD in cities across the country on World Kidney Day, March 14 and throughout the year. For locations and schedules, check out our calendar of events.

Source: http://www.kidney.org

Nutritional Adjuncts to the Fat-Soluble Vitamins A, D, and K .


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The “K” in “vitamin K” stands for “koagulation,” the German word for blood clotting. From its discovery in the 1930s through the late 1970s, we knew of no other roles for the vitamin.

The 1990s had come and nearly gone by the time awareness of its role in bone metabolism broke out of the confines of the vitamin K research community, and only in the twenty-first century has its role in preventing calcification of the blood vessels and other soft tissues become clear.

Vitamin K2, found in animal fats and fermented foods, is present in much smaller quantities in most diets when compared to vitamin K1, found in leafy greens.

Since researchers throughout the twentieth century saw the two forms of the vitamin as interchangeable, they ignored vitamin K2 as though its scarcity made it irrelevant.

The realization that vitamin K is not just for “koagulation,” however, led us to discover that vitamins K1 and K2 are not interchangeable after all: vitamin K1 more effectively supports blood clotting, while vitamin K2 more effectively ensures that calcium winds up in the bones and teeth where it supports health rather than in the soft tissues where it contributes to disease.

It was thus only in 2006 that the United States Department of Agriculture determined the vitamin K2 contents of common foods for the first time.1

Vitamins A, D, and K

While vitamin K2 languished in obscurity, vitamins A and D continually traded places with one another as the favored vitamin du jour. The pendulum initially swung in favor of vitamin D because rickets was common in the early twentieth century while eye diseases resulting from vitamin A deficiency were rare. It then swung in favor of vitamin A when that vitamin became known as the “anti-infective” vitamin.2

After World War II, the medical establishment had easy access to antibiotics and thus lost interest in battling infections with vitamin A.3 Vitamin D fared far worse, taking the blame for a British epidemic of infant hypercalcemia and eventually earning a reputation as “the most toxic of all the vitamins.”4 These days, the pendulum has swung full force in the opposite direction: we blame an epidemic of osteoporosis on vitamin A, and see vitamin D as the new panacea.5

Though a paradigm of synergy never took hold, it was not for want of opportunity. When Mellanby and Green first demonstrated in the 1920s that vitamin A prevented infections, they concluded that vitamin D could not be “safely substituted for cod-liver oil in medical treatment,” and that “if a substitute for cod-liver oil is given it ought to be at least as powerful as this oil in its content of both vitamins A and D.”

Consistent with this point of view, clinical trials in the 1930s showed that cod liver oil could reduce the incidence of colds by a third and cut hours missed from work in half.6 Cod liver oil also caused dramatic reductions in mortality from less common but more severe infections. The medical establishment, for example, had been successfully using it to treat tuberculosis since the mid-nineteenth century.7

Studies in the 1930s expanded this to the treatment of measles.8 These findings made the popularity of cod liver oil soar .

The idea that vitamin A alone was “antiinfective,” however, led to similar trials with halibut liver oil, which is rich in vitamin A but poor in vitamin D. These trials often failed to show any benefit. I.G. Spiesman of the University of Illinois College of Medicine proposed a simple solution to this paradox: vitamins A and D worked together to prevent infection, he suggested, and both vitamins are needed to prevent the common cold.

He published his own clinical trial in 1941, showing that massive doses of each vitamin alone provided no benefit and often proved toxic. Massive doses of both vitamins together, however, caused no toxicity and offered powerful protection against the common cold.10 Nevertheless, as antibiotics grew in popularity after World War II, interest in the fat-soluble vitamins waned and cod liver oil use began its steady decline .

The emergence of molecular biology in the late twentieth century provided new evidence for synergy. Vitamins A and D both make independent contributions to immune function by binding to their respective receptors and thereby directing cellular processes in favor of healthful immune responses, but studies in isolated cells suggest that vitamin D may only be able to activate its receptor with the direct cooperation of vitamin A.11, 12

We now know that vitamins A and D also cooperate together to regulate the production of certain vitamin K-dependent proteins. Once vitamin K activates these proteins, they help mineralize bones and teeth, support adequate growth, and protect arteries and other soft tissues from abnormal calcification, and protect against cell death.

As described below, the synergistic action of the fat-soluble trio depends on support from other nutrients like magnesium, zinc, fat and carbohydrate, as well as important metabolic factors such as carbon dioxide and thyroid hormone

Magnesium and the Fat-Soluble Vitamins

Magnesium contributes to more than three hundred specific chemical reactions that occur within our bodies, including every reaction that depends on ATP, the universal energy currency of our cells.13 Magnesium also activates the enzyme that makes copies of DNA, as well as the enzyme that makes RNA, which is responsible for translating the codes contained within our genes into the production of every protein within our body. This process of translating the DNA code in order to produce proteins is called “gene expression.”

Vitamins A and D carry out most of their functions by regulating gene expression, which means they rely directly on magnesium to carry out these functions. They also rely indirectly on magnesium because our cells can only produce their receptors and all the proteins with which they interact with the assistance of this critical mineral.

The well-studied interaction of magnesium with vitamin D and calcium provides an illustrative example. Magnesium is required for both steps in the activation of vitamin D to calcitriol, the form of vitamin D that regulates gene expression and stimulates calcium absorption. Even fully activated vitamin D (calcitriol), however, is useless in the absence of magnesium. Humans who are deficient in magnesium have low blood levels of both calcitriol and calcium, but treating them with calcitriol does nothing to restore calcium levels to normal. The only way to normalize calcium levels in these subjects is to provide them with sufficient magnesium. Magnesium also supports the cellular pumps that keep most calcium out of our soft tissue cells and make it available for the extracellular matrix of bones and teeth.

Zinc and the Fat-Soluble Vitamins

As with magnesium, the fat-soluble trio can only support health if our diets contain adequate zinc. The interaction between vitamin A and zinc is particularly well studied.15 Vitamin A supports the intestinal absorption of zinc, possibly by increasing the production of a binding protein in the intestines. Zinc, in turn, supports the formation of vesicles involved in transporting vitamin A and the other the fat-soluble vitamins across the intestinal wall.

Zinc is an essential structural component of many vitamin A-related proteins, including the primary protein that transports vitamin A through the blood, the enzyme that carries out the first step in the activation of vitamin A to retinoic acid, and the nuclear receptor that binds to retinoic acid and allows it to regulate gene expression.

Numerous studies have demonstrated the interaction between zinc and vitamin A in humans. For example, in humans with marginal zinc status, zinc supplementation supports vitamin A’s role in visual function16 and eye development (Figure 2).17

Although less well studied, zinc also interacts with vitamin D. Vitamin D and zinc most likely promote each other’s intestinal absorption.18 In rats, dietary zinc supports the production of the vitamin D receptor.19 Once the receptor is formed, zinc provides it with essential structural support. Although in the absence of this structural support the receptor still binds to vitamin D, the structural support is needed to allow this vitamin-receptor complex to bind to DNA.20 Studies with isolated cells illustrate the importance of this interaction: adding zinc to these cells increases the rate at which vitamin D activates the expression of genes.21

Fat, Carbs, Thyroid and Carbon Dioxide

In order to absorb fat-soluble vitamins from our food, we need to eat fat. Human studies show that both the amount and type of fat are important. For example, one study showed that absorption of beta-carotene from a salad with no added fat was close to zero. The addition of a lowfat dressing made from canola oil increased absorption, but a high-fat dressing was much more effective.23 Canola oil, however, is far from ideal. Studies in rats show that absorption of carotenoids is much higher with olive oil than with corn oil.24

Similarly, studies in humans show that consuming beta-carotene with beef tallow rather than sunflower oil increases the amount we absorb from 11 to 17 percent. The reason for this is unknown, but it may be that oils rich in polyunsaturated fatty acids promote the oxidative destruction of fat-soluble vitamins in the intestines before we are able to absorb them. Thus, the more fat we eat, and the lower those fats are in polyunsaturated fatty acids, the more fat-soluble vitamins we absorb.

While dietary fat is clearly important, there may be a role for dietary carbohydrate as well. Once vitamins A and D stimulate the production of vitamin K-dependent proteins, vitamin K activates those proteins by adding carbon dioxide to them. Once added to a protein, carbon dioxide carries a negative charge and allows the protein to interact with calcium, which carries a positive charge. The greater the supply of carbon dioxide, the better vitamin K can do its job.25 Carbohydrates are rich in carbon and oxygen, and when we break them down for energy we release these elements in our breath as carbon dioxide. Because carbohydrates are richer in oxygen, burning them generates about 30 percent more carbon dioxide per calorie than burning fat, and low-carbohydrate diets have been shown to lower blood levels of carbon dioxide .

Ideally, we should study this further by determining whether dietary carbohydrate affects the amount of activated vitamin K-dependent proteins in humans.

We also produce more carbon dioxide when we burn more calories, regardless of whether we are burning carbohydrate or fat. Intense exercise more than doubles the amount of carbon dioxide we produce compared to what we produce when at rest.27 Even working at a standing desk rather than a sitting desk increases both calories burned and carbon dioxide generated by about a third .

Future studies should directly investigate whether exercise increases the activation of vitamin K-dependent proteins, but it seems reasonable to suggest that part of the reason exercise promotes cardiovascular health may be because it ensures a more abundant supply of carbon dioxide, which vitamin K uses to activate proteins that protect our heart valves and blood vessels from calcification. Thyroid hormone is a key regulator of the metabolic rate and may thus be a major determinant of the carbon dioxide available for activating vitamin K-dependent proteins. Theoretically, thyroid hormone should increase the rate of metabolism and a greater rate of metabolism should produce a proportionally greater supply of carbon dioxide.

Thyroid hormone directly increases the production of vitamin K-dependent proteins and protects blood vessels from calcification in rats.29 The reason for this relationship is unclear. We could speculate, however, that our bodies in their infinite wisdom use thyroid hormone to tie the production of vitamin K-dependent proteins to the production the carbon dioxide needed to activate them.

The Big Picture

It is clearly time to move beyond viewing each vitamin in isolation. The fat-soluble vitamins not only synergize with each other, but cooperate with many other nutrients and metabolic factors such as magnesium, zinc, fat, carbohydrate, carbon dioxide and thyroid hormone.

This paradigm has two important implications. At the level of scientific research, a study about one vitamin can easily come to false conclusions unless it takes into account its interactions with all the others. We should reverently and humbly bow before the complexity of these interactions, realizing how little we know and recognizing that we are always learning. At the level of personal health, these interactions emphasize the need to consume a well-rounded, nutrient-dense diet. Supplementation with an individual vitamin runs the risk of throwing it out of balance with its synergistic partners. The fat-soluble vitamins work most safely and effectively when we obtain them from natural foods within the context of a diet rich in all their synergistic partners.

Zinc and the Dark Adaptation Test for Vitamin A Deficiency

The role of vitamin A in vision is unusual. This vitamin carries out most of its known actions by regulating the expression of specific sets of genes. Vitamin A regulates gene expression only after being activated in a two-step process from retinol to retinal, and finally to retinoic acid. Vitamin A supports vision, however, in its semi-activated form as retinal. Retinal binds to a protein known as opsin, forming a vitamin-protein complex known as rhodopsin. Each photon of light that enters our eye and collides with rhodopsin causes the retinal to change shape and release itself from the complex. This event then translates into an electrical impulse that our optic nerve transmits to our brain. The brain synthesizes myriad such electrical impulses at every moment and interprets them as vision.30

While the function of opsin is to help generate visual images by binding and releasing vitamin A, opsin can only maintain its proper shape and function when it is bound to zinc. In addition, zinc supports the conversion of retinol to retinal, the form of vitamin A that binds to opsin. We could predict, then, that vitamin A would only be able to support vision in the presence of adequate zinc. This can be studied by determining dark adaptation thresholds, which determine the dimmest spots of light we are able to see after having spent a period of time in the dark to maximize our visual sensitivity. When vitamin A is insufficient, we lose the ability to see the dimmer spots of light.

Robert Russell of Tufts University studied ten patients with deficient blood levels of vitamin A who also failed the dark-adaptation test. Eight of them achieved normal dark-adaptation thresholds after supplementing with 10,000 international units of vitamin A for two to four weeks. Two of them, however, had deficient blood levels of zinc. Vitamin A supplementation alone failed to normalize their visual function, but adding 220 milligrams per day of zinc to the regimen for two weeks brought it back to normal.16 These results show that vitamin A can only support healthy vision with the direct assistance of zinc.

Source: mercola.com

Venous Angioplasty Fails to Help MS Patients in First Randomized Trial .


Percutaneous transluminal venous angioplasty is ineffective in correcting chronic cerebrospinal venous insufficiency in patients with multiple sclerosis, according to the first randomized trial of the procedure, presented at the American Academy of Neurology‘s annual meeting.

Researchers studied venous angioplasty in 10 patients with MS in an open-label safety assessment, after which they randomized 19 patients to either angioplasty or a sham control. Primary outcomes included safety at 1 day and 1 month, venous outflow restoration, and new lesion activity and relapse over 6 months.

The researchers concluded that the procedure is not only ineffective but also may exacerbate MS disease activity in the short-term.

Source: American Academy of Neurology meeting website

Patient Caught Rabies Through Organ Transplant, CDC Says.


A patient who recently died of rabies in Maryland contracted the illness from a kidney transplant received over a year ago, the CDC reported on Friday. The lengthy incubation period, while longer than the typical 1 to 3 months, is unusual but not unprecedented.

Tests on tissue samples from the patient and donor confirmed that they were both infected with raccoon-type rabies. The three other patients who received organs from the donor have been identified and are receiving anti-rabies shots.

The CDC notes: “If rabies is not clinically suspected [in a potential donor], laboratory testing for rabies is not routinely performed, as it is difficult for doctors to confirm results in the short window of time they have to keep the organs viable for the recipient.”

Source: CDC

Aspirin May Prevent Melanoma in Postmenopausal White Women.


Regular aspirin use is associated with a reduction in melanoma risk among postmenopausal white women, according to an analysis from the Women’s Health Initiative Observational Study, published in Cancer.

Researchers followed nearly 60,000 women for a median of 12 years. During that time, some 550 melanomas were diagnosed. Women who reported using aspirin regularly had a 21% lower incidence of melanoma than those taking nonaspirin NSAIDs or those not taking NSAIDs.

In Journal Watch Dermatology, Jeffrey P. Callen writes: “Unless there is a contraindication, I will tell a patient who asks my advice that low-dose aspirin seems to usefully reduce melanoma risk.”

Source: Journal Watch Dermatology summary

Some Patients with HIV Treated Early Keep Very Low Viral Loads Even After Stopping Therapy.


 

Some patients treated early in HIV infection may be able to maintain very low-to-undetectable viral loads years after stopping antiretroviral therapy, a PLoS Pathogens study finds.

Researchers studied 14 patients whose treatment with combination antiretrovirals began soon after exposure to HIV. The patients’ viral loads became undetectable within roughly 3 months, and treatment was interrupted after about 3 years.

The patients were found to have very low viral loads and stable CD4-cell counts after several years without therapy. The researchers estimate that about 15% of those treated early could achieve similar results.

Asked to comment, Paul Sax of Journal Watch HIV/AIDS Clinical Care wrote: “For the small minority of patients diagnosed with HIV very early after HIV acquisition, these data provide additional support that aggressive early therapy is warranted.”

Source: PLOS

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